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485 results on '"A La Spada"'

1. Chronic BMAA exposure combined with TDP-43 mutation elicits motor neuron dysfunction phenotypes in mice

Author: F.J. Arnold, M. Burns, Y. Chiu, J. Carvalho, A.D. Nguyen, P.C. Ralph, A.R. La Spada, and C.L. Bennett
Subjects: Aging, General Neuroscience, Neurology (clinical), Geriatrics and Gerontology, Developmental Biology
Published: 2023

2. Financial Sanctions, SWIFT, and the Architecture of the International Payment System

Author: Marco Cipriani, Linda S. Goldberg, and Gabriele La Spada
Subjects: Economics and Econometrics, Mechanical Engineering, Energy Engineering and Power Technology, Management Science and Operations Research
Abstract: Financial sanctions, alongside economic sanctions, are components of the toolkit used by governments as part of international diplomacy. The use of sanctions, especially financial, has increased over the last 70 years. Financial sanctions have been particularly important whenever the goals of the sanctioning countries were related to democracy and human rights. Financial sanctions restrict entities—countries, businesses, or even individuals—from purchasing or selling financial assets, or from accessing custodial or other financial services. They can be imposed on a sanctioned entity’s ability to access the infrastructures that are in place to execute international payments, irrespective of whether such payments underpin financial or real activity. This article explains how financial sanctions can be designed to limit access to the international payment system and, in particular, the SWIFT network, and provides some recent examples.
Published: 2023

3. X-linked SBMA model mice display relevant non-neurological phenotypes and their expression of mutant androgen receptor protein in motor neurons is not required for neuromuscular disease

Author: Gromova, Anastasia, Cha, Byeonggu, Robinson, Erica M, Strickland, Laura M, Nguyen, Nhat, ElMallah, Mai K, Cortes, Constanza J, and La Spada, Albert R
Subjects: Motor Neurons, Male, Bulbo-Spinal Atrophy, Clinical Sciences, Neurosciences, X-Linked, Neurodegenerative, Transgenic, Androgen, Mice, Phenotype, Rare Diseases, Orphan Drug, Musculoskeletal, Nerve Degeneration, Receptors, Neurological, Genetics, Animals, Humans, 2.1 Biological and endogenous factors, Biochemistry and Cell Biology, Aetiology, Aged
Abstract: X-linked spinal and bulbar muscular atrophy (SBMA; Kennedy's disease) is a rare neuromuscular disorder characterized by adult-onset proximal muscle weakness and lower motor neuron degeneration. SBMA was the first human disease found to be caused by a repeat expansion mutation, as affected patients possess an expanded tract of CAG repeats, encoding polyglutamine, in the androgen receptor (AR) gene. We previously developed a conditional BAC fxAR121 transgenic mouse model of SBMA and used it to define a primary role for skeletal muscle expression of polyglutamine-expanded AR in causing the motor neuron degeneration. Here we sought to extend our understanding of SBMA disease pathophysiology and cellular basis by detailed examination and directed experimentation with the BAC fxAR121 mice. First, we evaluated BAC fxAR121 mice for non-neurological disease phenotypes recently described in human SBMA patients, and documented prominent non-alcoholic fatty liver disease, cardiomegaly, and ventricular heart wall thinning in aged male BAC fxAR121 mice. Our discovery of significant hepatic and cardiac abnormalities in SBMA mice underscores the need to evaluate human SBMA patients for signs of liver and heart disease. To directly examine the contribution of motor neuron-expressed polyQ-AR protein to SBMA neurodegeneration, we crossed BAC fxAR121 mice with two different lines of transgenic mice expressing Cre recombinase in motor neurons, and after updating characterization of SBMA phenotypes in our current BAC fxAR121 colony, we found that excision of mutant AR from motor neurons did not rescue neuromuscular or systemic disease. These findings further validate a primary role for skeletal muscle as the driver of SBMA motor neuronopathy and indicate that therapies being developed to treat patients should be delivered peripherally.
Published: 2023

4. Functional diversity of nanohaloarchaea within xylan-degrading consortia

Author: Reva, Oleg, Messina, Enzo, La Cono, Violetta, Crisafi, Francesca, Smedile, Francesco, La Spada, Gina, Marturano, Laura, Selivanova, Elena, Rohde, Manfred, Krupovic, Mart, Yakimov, Michail, University of Pretoria [South Africa], National Research Council of Italy | Consiglio Nazionale delle Ricerche (CNR), Institute of Polar Sciences [Venezia-Mestre] (CNR-ISP), Russian Academy of Sciences [Moscow] (RAS), Helmholtz Centre for Infection Research (HZI), Virologie des archées - Archaeal Virology, Université Paris Cité (UPCité)-Microbiologie Intégrative et Moléculaire (UMR6047), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), This study was supported by a grant from the FUTURENZYMES Project (Contract 101000327), funded by the European Union's Horizon 2020 Research Program. MK was supported by Agence Nationale de la Recherche grant ANR-20-CE20-0009. This work has been additionally supported by the project 'Emergence of virulence and antibiotic-resistance vectors in coastal and deep sea marine environments and analysis of the mechanisms and conditions underlying their spread and evolution' funded by the MIUR Progetti di Ricerca di Rilevante Interesse Nazionale (PRIN) Bando 2017 - grant 201728ZA49_001 and by the project 'Innovazione tecnologica per la tutela e valorizzazione degli ecosistemi marini (ITEM)' funded by MIUR CTN02_00059_9948371., and ANR-20-CE20-0009,VIROMET,Devoiler le virome des archées methanogenes(2020)
Subjects: Microbiology (medical), nanohaloarchaeal-haloarchaeal symbioses ecology of nanohaloarchaea CRISPR ncRNA methylomics, CRISPR, [SDV]Life Sciences [q-bio], nanohaloarchaeal-haloarchaeal symbioses, methylomics, ncRNA, Microbiology, ecology of nanohaloarchaea
Abstract: Extremely halophilic representatives of the phylum Candidatus Nanohaloarchaeota (members of the DPANN superphyla) are obligately associated with extremely halophilic archaea of the phylum Halobacteriota (according to the GTDB taxonomy). Using culture-independent molecular techniques, their presence in various hypersaline ecosystems around the world has been confirmed over the past decade. However, the vast majority of nanohaloarchaea remain uncultivated, and thus their metabolic capabilities and ecophysiology are currently poorly understood. Using the (meta)genomic, transcriptomic, and DNA methylome platforms, the metabolism and functional prediction of the ecophysiology of two novel extremely halophilic symbiotic nanohaloarchaea (Ca. Nanohalococcus occultus and Ca. Nanohalovita haloferacivicina) stably cultivated in the laboratory as members of a xylose-degrading binary culture with a haloarchaeal host, Haloferax lucentense, was determined. Like all known DPANN superphylum nanoorganisms, these new sugar-fermenting nanohaloarchaea lack many fundamental biosynthetic repertoires, making them exclusively dependent on their respective host for survival. In addition, given the cultivability of the new nanohaloarchaea, we managed to discover many unique features in these new organisms that have never been observed in nano-sized archaea both within the phylum Ca. Nanohaloarchaeota and the entire superphylum DPANN. This includes the analysis of the expression of organism-specific non-coding regulatory (nc)RNAs (with an elucidation of their 2D-secondary structures) as well as profiling of DNA methylation. While some ncRNA molecules have been predicted with high confidence as RNAs of an archaeal signal recognition particle involved in delaying protein translation, others resemble the structure of ribosome-associated ncRNAs, although none belong to any known family. Moreover, the new nanohaloarchaea have very complex cellular defense mechanisms. In addition to the defense mechanism provided by the type II restriction-modification system, consisting of Dcm-like DNA methyltransferase and Mrr restriction endonuclease, Ca. Nanohalococcus encodes an active type I-D CRISPR/Cas system, containing 77 spacers divided into two loci. Despite their diminutive genomes and as part of their host interaction mechanism, the genomes of new nanohaloarchaea do encode giant surface proteins, and one of them (9,409 amino acids long) is the largest protein of any sequenced nanohaloarchaea and the largest protein ever discovered in cultivated archaea.
Published: 2023

5. Clonally expanded CD8 T cells characterize amyotrophic lateral sclerosis-4

Author: Laura Campisi, Shahab Chizari, Jessica S. Y. Ho, Anastasia Gromova, Frederick J. Arnold, Lorena Mosca, Xueyan Mei, Yesai Fstkchyan, Denis Torre, Cindy Beharry, Marta Garcia-Forn, Miguel Jiménez-Alcázar, Vladislav A. Korobeynikov, Jack Prazich, Zahi A. Fayad, Marcus M. Seldin, Silvia De Rubeis, Craig L. Bennett, Lyle W. Ostrow, Christian Lunetta, Massimo Squatrito, Minji Byun, Neil A. Shneider, Ning Jiang, Albert R. La Spada, and Ivan Marazzi
Subjects: Motor Neurons, Multidisciplinary, General Science & Technology, Amyotrophic Lateral Sclerosis, DNA Helicases, Neurosciences, CD8-Positive T-Lymphocytes, Neurodegenerative, Multifunctional Enzymes, Article, Clone Cells, Brain Disorders, Mice, Rare Diseases, Mutation, Neurological, Genetics, Animals, 2.1 Biological and endogenous factors, Gene Knock-In Techniques, ALS, Aetiology, RNA Helicases
Abstract: Amyotrophic lateral sclerosis (ALS) is a heterogenous neurodegenerative disorder that affects motor neurons and voluntary muscle control1. ALS heterogeneity includes the age of manifestation, the rate of progression and the anatomical sites of symptom onset. Disease-causing mutations in specific genes have been identified and define different subtypes of ALS1. Although several ALS-associated genes have been shown to affect immune functions2, whether specific immune features account for ALS heterogeneity is poorly understood. Amyotrophic lateral sclerosis-4 (ALS4) is characterized by juvenile onset and slow progression3. Patients with ALS4 show motor difficulties by the time that they are in their thirties, and most of them require devices to assist with walking by their fifties. ALS4 is caused by mutations in the senataxin gene (SETX). Here, using Setx knock-in mice that carry the ALS4-causative L389S mutation, we describe an immunological signature that consists of clonally expanded, terminally differentiated effector memory (TEMRA) CD8 T cells in the central nervous system and the blood of knock-in mice. Increased frequencies of antigen-specific CD8 T cells in knock-in mice mirror the progression of motor neuron disease and correlate with anti-glioma immunity. Furthermore, bone marrow transplantation experiments indicate that the immune system has a key role in ALS4 neurodegeneration. In patients with ALS4, clonally expanded TEMRA CD8 T cells circulate in the peripheral blood. Our results provide evidence of an antigen-specific CD8 T cell response in ALS4, which could be used to unravel disease mechanisms and as a potential biomarker of disease state.
Published: 2022

6. Astrocytic LRRK2 Controls Synaptic Connectivity through ERM Phosphorylation

Author: Shiyi Wang, Dhanesh Sivadasan Bindu, Christabel Xin Tan, Kristina Sakers, Tetsuya Takano, Maria Pia Rodriguez, Kylie Dimond, Scott H. Soderling, Albert R. La Spada, and Cagla Eroglu
Abstract: Astrocytes tightly control neuronal connectivity and function in the brain through direct contact with synapses1–5. These glial cells become reactive during disease pathogenesis6–8including Parkinson’s disease (PD)9–14. However, it remains unknown if astrocyte dysfunction is an initiating factor of PD pathogenesis and whether astrocytes can be targeted to stop or reverse the synaptic dysfunction seen in PD. Usingin vitroandin vivomethods, we found that the PD-linked gene Lrrk2 controls astrocyte morphology via regulating the phosphorylation of ERM proteins (Ezrin, Radixin, and Moesin), a structural component of the perisynaptic astrocyte processes. ERM phosphorylation is robustly elevated both in mice and humans carrying the LRRK2 G2019S Parkinsonism mutation. Importantly, the reduction of the ERM phosphorylation, specifically in the LRRK2 G2019S in adult astrocytes, is sufficient to restore excitatory synapse number and function deficits in the LRRK2 G2019S knock-in mouse cortex. These results show a role for Lrrk2 in controlling astrocyte morphogenesis and synaptogenic function and reveal that early astrocyte dysfunction in PD could be causal to disruptions in cortical excitatory synaptic connectivity. The astrocytic dysfunction can be corrected by dampening ERM phosphorylation, pinpointing astrocytes as critical cellular targets for PD therapeutics.
Published: 2023

7. Purkinje-Enriched snRNA-seq in SCA7 Cerebellum Reveals Zebrin Identity Loss as a Central Feature of Polyglutamine Ataxias

Author: Luke C. Bartelt, Pawel M. Switonski, Grażyna Adamek, Juliana Carvalho, Lisa A. Duvick, Sabrina I. Jarrah, Hayley S. McLoughlin, Daniel R. Scoles, Stefan M. Pulst, Harry T. Orr, Court Hull, Craig B. Lowe, and Albert R. La Spada
Abstract: Spinocerebellar ataxia type 7 (SCA7) is an inherited neurodegenerative disorder caused by a CAG-polyglutamine repeat expansion. SCA7 patients display a striking loss of Purkinje cell (PC) neurons with disease progression; however, PCs are rare, making them difficult to characterize. We developed a PC nuclei enrichment protocol and applied it to single-nucleus RNA-seq of a SCA7 knock-in mouse model. Our results unify prior observations into a central mechanism of cell identity loss, impacting both glia and PCs, driving accumulation of inhibitory synapses and altered PC spiking. Zebrin-II subtype dysregulation is the predominant signal in PCs, leading to complete loss of zebrin-II striping at motor symptom onset in SCA7 mice. We show this zebrin-II subtype degradation is shared across Polyglutamine Ataxia mouse models and SCA7 patients. It has been speculated that PC subtype organization is critical for cerebellar function, and our results suggest that a breakdown of zebrin-II parasagittal striping is pathological.
Published: 2023

8. Antibacterial Properties of AquaSun Sol-Gel Coating

Author: Francesca Crisafi, Mario Pagliaro, Gina La Spada, Violetta Lo Cono, Laura Marturano, Cristina Scolaro, Francesco Smedile, Annamaria Visco, and Rosaria Ciriminna
Abstract: We investigate the antimicrobial activity, surface features, wettability and adhesion of photocatalytic xerogel AquaSun deposited on shipbuilding steel, in comparison to those of a commercial antifouling paint. Evaluated exposing the surface of shipbuilding steel pre-treated with primer and tie coat paint, and further coated with a thin layer of AquaSun to a microbial consortium composed by Bacillus aquimaris DSM 16205T and Pseudomonas poae DSM 14936T, the antimicrobial activity is both significant and of broad scope. Taking into account also the low cost, high stability and lack of eco-toxicity of this hybrid sol-gel coating, these results are promising en route to developing novel antimicrobial coatings of broad applicability.
Published: 2023

9. Alternative polyadenylation transcriptome-wide association study identifies APA-linked susceptibility genes in brain disorders

Author: Ya Cui, Frederick J. Arnold, Fanglue Peng, Dan Wang, Jason Sheng Li, Sebastian Michels, Eric J. Wagner, Albert R. La Spada, and Wei Li
Subjects: Multidisciplinary, General Physics and Astronomy, General Chemistry, General Biochemistry, Genetics and Molecular Biology
Abstract: Alternative polyadenylation (APA) plays an essential role in brain development; however, current transcriptome-wide association studies (TWAS) largely overlook APA in nominating susceptibility genes. Here, we performed a 3′ untranslated region (3′UTR) APA TWAS (3′aTWAS) for 11 brain disorders by combining their genome-wide association studies data with 17,300 RNA-seq samples across 2,937 individuals. We identified 354 3′aTWAS-significant genes, including known APA-linked risk genes, such as SNCA in Parkinson’s disease. Among these 354 genes, ~57% are not significant in traditional expression- and splicing-TWAS studies, since APA may regulate the translation, localization and protein-protein interaction of the target genes independent of mRNA level expression or splicing. Furthermore, we discovered ATXN3 as a 3′aTWAS-significant gene for amyotrophic lateral sclerosis, and its modulation substantially impacted pathological hallmarks of amyotrophic lateral sclerosis in vitro. Together, 3′aTWAS is a powerful strategy to nominate important APA-linked brain disorder susceptibility genes, most of which are largely overlooked by conventional expression and splicing analyses.
Published: 2023

10. Financial Sanctions, SWIFT, and the Architecture of the International Payments System

Author: Marco Cipriani, Linda S. Goldberg, and Gabriele La Spada
Subjects: History, Polymers and Plastics, Business and International Management, Industrial and Manufacturing Engineering
Published: 2023

11. Spinocerebellar Ataxia Type 7: From Mechanistic Pathways to Therapeutic Opportunities

Author: Pawel M. Switonski and Albert R. La Spada
Published: 2023

12. Novel benzothiazole derivatives as multitargeted-directed ligands for the treatment of Alzheimer’s disease

Author: Donia E. Hafez, Mariam Dubiel, Gabriella La Spada, Marco Catto, David Reiner-Link, Yu-Ting Syu, Mohammad Abdel-Halim, Tsong-Long Hwang, Holger Stark, and Ashraf H. Abadi
Subjects: Pharmacology, Drug Discovery, General Medicine
Abstract: Neurodegenerative diseases such as Alzheimer’s disease (AD) are multifactorial with several different pathologic mechanisms. Therefore, it is assumed that multitargeted-directed ligands (MTDLs) which interact with different biological targets relevant to the diseases, might offer an improved therapeutic alternative than using the traditional “one-target, one-molecule” approach. Herein, we describe new benzothiazole-based derivatives as a privileged scaffold for histamine H3 receptor ligands (H3R). The most affine compound, the 3-(azepan-1-yl)propyloxy-linked benzothiazole derivative 4b, displayed a Ki value of 0.012 μM. The multitargeting potential of these H3R ligands towards AChE, BuChE and MAO-B enzymes was evaluated to yield compound 3s (pyrrolidin-1-yl-(6-((5-(pyrrolidin-1-yl)pentyl)oxy)benzo[d]thiazol-2-yl)methanone) as the most promising MTDL with a Ki value of 0.036 μM at H3R and IC50 values of 6.7 µM, 2.35 µM, and 1.6 µM towards AChE, BuChE, and MAO-B, respectively. These findings suggest that compound 3s can be a lead structure for developing new multi-targeting anti-AD agents.
Published: 2023
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13. Additional file 1 of X-linked SBMA model mice display relevant non-neurological phenotypes and their expression of mutant androgen receptor protein in motor neurons is not required for neuromuscular disease

Author: Gromova, Anastasia, Cha, Byeonggu, Robinson, Erica M., Strickland, Laura M., Nguyen, Nhat, ElMallah, Mai K., Cortes, Constanza J., and La Spada, Albert R.
Abstract: Additional file 1. Figure S1: Characterization of body weight of male wildtype and HSA-Cre only controls compared to singly transgenic BAC fxAR121 and muscle-rescued BAC fxAR121;HSA-Cre mice. A) Weight of individual animals of each genotype plotted as a function of time and fitted with a simple linear regression. Slopes and R squared values are as follows: wildtype, HSA-Cre, HSA/fxAR121, fxAR121. B) Gross anatomical analysis upon dissection of agedmale mice showing robust inguinal, epidydimal, and mesenteric white adipose deposits in control miceand the complete absence of these deposits in BAC fxAR121; HSA-Cre mice.
Published: 2023
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14. Costly Concessions, Internally Divided Movements, and Strategic Repression: A Movement-Level Analysis

Author: Eleonora La Spada
Subjects: Sociology and Political Science, Political Science and International Relations
Abstract: Is government repression of self-determination (SD) movements affected by the internal structure of the movements? This article investigates the relation between internal fragmentation of SD movements and state repression. While internal fragmentation of domestic challengers is well-documented in conflict studies, its effect on state repression is largely overlooked by the extant literature. Here, I argue that inter-faction competition and disagreements within an internally divided movement constrain the government's ability to negotiate concessions in a way that can satisfy all the actors involved, engendering incentives to repress the movement. I expect that the degree to which this mechanism operates depends on the extent to which the movement is internally fragmented. The findings show that higher degrees of within-movement fragmentation are positively associated with higher levels of repression, and this effect is greater in the presence of active violent militants but smaller in the presence of one or a few dominant faction(s). This study sheds light on the mechanisms that drive repression over SD disputes, which often lead to escalation of violence and civil conflict onset. A deeper understanding of these mechanisms can help with the development of early warning systems and conflict prevention in the political practice of national and international organizations.
Published: 2022

15. Towards Alzheimer's disease-related targets: One-pot Cu(I)- mediated synthesis of new nitroindazolyltriazoles

Author: Mohammed Eddahmi, Gabriella La Spada, Abderrafia Hafid, Mostafa Khouili, Marco Catto, and Latifa Bouissane
Subjects: Indazoles, Alzheimer Disease, Organic Chemistry, Drug Discovery, Brain, Cholinesterases, Amyloidogenic Proteins, Triazoles, Molecular Biology, Biochemistry, Monoamine Oxidase, Copper, Catalysis
Abstract: In this work, we have investigated the one pot strategy for the Cu(I)-mediated synthesis of new triazoles bearing nitroindazole moieties using different copper catalysts. The biological activity of newly synthesized nitroindazolyltriazoles towards Alzheimer's disease-related targets, namely cholinesterases, monoamine oxidases, and amyloid aggregation, were investigated. Predictions of target affinity, physicochemical parameters, gastrointestinal absorption and brain penetration were achieved by means of in silico tools.
Published: 2022

16. Bioisosteric replacement based on 1,2,4-oxadiazoles in the discovery of 1H-indazole-bearing neuroprotective MAO B inhibitors

Author: Mariagrazia Rullo, Gabriella La Spada, Daniela Valeria Miniero, Andrea Gottinger, Marco Catto, Pietro Delre, Margherita Mastromarino, Tiziana Latronico, Sara Marchese, Giuseppe Felice Mangiatordi, Claudia Binda, Anna Linusson, Grazia Maria Liuzzi, and Leonardo Pisani
Subjects: Pharmacology, Organic Chemistry, Drug Discovery, General Medicine
Published: 2023

17. Protocol for mapping double-stranded DNA break sites across the genome with translocation capture sequencing

Author: Delaney, Joe R. and La Spada, Albert R.
Subjects: General Immunology and Microbiology, General Neuroscience, Protocol, General Biochemistry, Genetics and Molecular Biology
Abstract: Translocation sequencing can be used to assess mechanisms of DNA repair and identify genome-wide double-strand breaks (DSBs) accessible to DNA repair machinery. Here, we present a protocol for mapping double-strand DNA break sites across the genome with translocation capture sequencing. Bait DSBs are introduced using a Cas9 nuclease and repaired by the host cell, connecting bait DSBs to other DSBs. Repair sites are detected by isolating bait site DNA, cleaving normal sequence to enrich off-site repair, and next-generation sequencing. For complete details on the use and execution of this protocol, please refer to Switonski et al. (2021).(1)
Published: 2023

18. A super absorbent polymer containing copper to control

Author: Soumia, El Boumlasy, Federico, La Spada, Antonella, Pane, Antonino, Licciardello, Abderrahmane, Debdoubi, Nunzio, Tuccitto, and Santa Olga, Cacciola
Abstract: The aim of this study was to determine the effectiveness of a Super absorbent polymer (SAP) containing copper (SAP-Cu) in controlling mal secco disease (MSD) of lemon caused by the fungus
Published: 2022

19. Investors’ appetite for money-like assets: The MMF industry after the 2014 regulatory reform

Author: Gabriele La Spada and Marco Cipriani
Subjects: 040101 forestry, Economics and Econometrics, Government, 050208 finance, Strategy and Management, 05 social sciences, Monetary theory, 04 agricultural and veterinary sciences, Monetary economics, Regulatory reform, Commission, Prime (order theory), Information sensitivity, Basis point, Accounting, 0502 economics and business, 0401 agriculture, forestry, and fisheries, Business, Money market fund, Finance
Abstract: This paper uses a quasi-natural experiment to estimate the premium for money-likeness. The 2014 Securities and Exchange Commission (SEC) reform of the money market fund (MMF) industry reduced the money-likeness of prime MMFs by increasing their information sensitivity, while leaving government MMFs unaffected. Investors fled from prime to government MMFs, with total outflows exceeding one trillion dollars. Using a difference-in-differences design, we estimate the premium for money-likeness to be between 20 and 30 basis points (bps). These premiums are not due to changes in investors’ risk tolerance or funds’ risk taking. Our results support recent developments in monetary theory identifying information insensitivity as a key feature of money.
Published: 2021

20. Skeletal Muscle Proteostasis Promotes Central Nervous System Rejuvenation and Reduces Neuroinflammation during Aging and Neurodegenerative Disease

Author: Ian Matthews, Allison Birnbaum, Anastasia Gromova, Kristen Coutinho, Megan McGraw, Dalton Patterson, Macy T. Banks, Amber Nobles, Nhat Nguyen, Helen C. Miranda, Albert R. La Spada, and Constanza J. Cortes
Abstract: Skeletal muscle has recently arisen as a novel regulator of Central Nervous System (CNS) function and aging, secreting bioactive molecules known as myokines with proteostasis and metabolism-modifying functions in targeted tissues, including the CNS. Here we report the generation of a novel transgenic mouse with enhanced skeletal muscle proteostasis via moderate overexpression of master regulator of proteostasis and lysosomal function Transcription Factor E-B. We have discovered that the resulting enhanced muscle proteostasis function significantly ameliorates proteotoxicity, reduces neuroinflammation and promotes transcriptional remodeling of the aging CNS, preserving cognition and memory in aging mice. Enhancing skeletal muscle proteostasis also reduces neuroinflammation and accumulation of tau-associated pathological hallmarks in a mouse model of tau pathology. Our results implicate maintenance of skeletal muscle proteostasis throughout aging to direct regulations of the aging CNS metabolism and function, and suggest that skeletal-muscle originating factors may act as novel therapeutic targets against age-associated neurodegenerative diseases.
Published: 2022

21. Skeletal Muscle Proteostasis Promotes Central Nervous System Function and Reduces Neuroinflammation during Aging and Neurodegenerative Disease

Author: Ian Matthews, Allison Birnbaum, Anastasia Gromova, Kristen Coutinho, Megan McGraw, Dalton C. Patterson, Macy T. Banks, Amber Nobles, Nhat Nguyen, Helen C. Miranda, Albert R. La Spada, and Constanza J. Cortes
Abstract: Skeletal muscle has recently arisen as a novel regulator of Central Nervous System (CNS) function and aging, secreting bioactive molecules known as myokines with proteostasis and metabolism-modifying functions in targeted tissues, including the CNS. Here we report the generation of a novel transgenic mouse with enhanced skeletal muscle proteostasis via targeted overexpression of Transcription Factor E-B, a master regulator of proteostasis and lysosomal function. We have discovered that the resulting enhanced muscle proteostasis function significantly ameliorates proteotoxicity, reduces neuroinflammation and promotes transcriptional remodeling of the aging CNS, preserving cognition and memory in aging mice. Enhancing skeletal muscle proteostasis also reduces neuroinflammation and accumulation of tau-associated pathological hallmarks in a mouse model of tau pathology. Our results implicate the maintenance of skeletal muscle proteostasis throughout aging to direct regulation of the CNS metabolism and function, and suggest that skeletal-muscle originating factors may act as novel therapeutic targets against age-associated neurodegenerative diseases.
Published: 2022

22. DNA Metabarcoding and Isolation by Baiting Complement Each Other in Revealing

Author: Federico, La Spada, Peter J A, Cock, Eva, Randall, Antonella, Pane, David E L, Cooke, and Santa Olga, Cacciola
Abstract: Isolation techniques supplemented by sequencing of DNA from axenic cultures have provided a robust methodology for the study of
Published: 2022

23. Wintertime Simulations Induce Changes in the Structure, Diversity and Function of Antarctic Sea Ice-Associated Microbial Communities

Author: Violetta La Cono, Francesco Smedile, Francesca Crisafi, Laura Marturano, Stepan V. Toshchakov, Gina La Spada, Ninh Khắc Bản, and Michail M. Yakimov
Subjects: Microbiology (medical), Virology, Antarctica, sea-ice brine, microbial community, SIMCO, sulfate-reducing bacteria, sulfur-oxidizing bacteria, SSU gene amplicon sequencing, Microbiology
Abstract: Antarctic sea-ice is exposed to a wide range of environmental conditions during its annual existence; however, there is very little information describing the change in sea-ice-associated microbial communities (SIMCOs) during the changing seasons. It is well known that during the solar seasons, SIMCOs play an important role in the polar carbon-cycle, by increasing the total photosynthetic primary production of the South Ocean and participating in the remineralization of phosphates and nitrogen. What remains poorly understood is the dynamic of SIMCO populations and their ecological contribution to carbon and nutrient cycling throughout the entire annual life of Antarctic sea-ice, especially in winter. Sea ice at this time of the year is an extreme environment, characterized by complete darkness (which stops photosynthesis), extremely low temperatures in its upper horizons (down to −45 °C) and high salinity (up to 150–250 psu) in its brine inclusions, where SIMCOs thrive. Without a permanent station, wintering expeditions in Antarctica are technically difficult; therefore, in this study, the process of autumn freezing was modelled under laboratory conditions, and the resulting ‘young ice’ was further incubated in cold and darkness for one month. The ice formation experiment was primarily designed to reproduce two critical conditions: (i) total darkness, causing the photosynthesis to cease, and (ii) the presence of a large amount of algae-derived organic matter. As expected, in the absence of photosynthesis, the activity of aerobic heterotrophs quickly created micro-oxic conditions, which caused the emergence of new players, namely facultative anaerobic and anaerobic microorganisms. Following this finding, we can state that Antarctic pack-ice and its surrounding ambient (under-ice seawater and platelet ice) are likely to be very dynamic and can quickly respond to environmental changes caused by the seasonal fluctuations. Given the size of Antarctic pack-ice, even in complete darkness and cessation of photosynthesis, its ecosystem appears to remain active, continuing to participate in global carbon-and-sulfur cycling under harsh conditions.
Published: 2022

24. Symbiosis between nanohaloarchaeon and haloarchaeon is based on utilization of different polysaccharides

Author: Stepan V. Toshchakov, Dimitry Y. Sorokin, Renata Denaro, Manuel Ferrer, Peter N. Golyshin, Francesca Crisafi, Gina La Spada, Erika Arcadi, Laura Giuliano, Michail M. Yakimov, Manfred Rohde, Enzo Messina, Olga V. Golyshina, Sergio Ciordia, John E. Hallsworth, María Carmen Mena, Alexander Y. Merkel, Violetta La Cono, Francesco Smedile, Margarita A. Shevchenko, Ministero dell'Istruzione, dell'Università e della Ricerca, Welsh Government, Ministry of Education, Culture and Science (The Netherlands), Russian Foundation for Basic Research, and Ministry of Education and Science of the Russian Federation
Subjects: Archaeal Proteins, Polysaccharide utilization, Biology, Polysaccharide, Microbiology, Nanohaloarchaea, chemistry.chemical_compound, Chitin, Symbiosis, Genome, Archaeal, Polysaccharides, Solar salterns, Halomicrobium, General, Phylogeny, haloarchaea, chemistry.chemical_classification, Halobacteriaceae, Multidisciplinary, Glycogen, Haloarchaea, Genomics, Biological Sciences, biology.organism_classification, Coculture Techniques, symbiosis, solar salterns, chemistry, Biochemistry, nanohaloarchaea, Nanoarchaeota, Candidatus, Gene Expression Regulation, Archaeal, polysaccharide utilization
Abstract: © 2020 the Author(s)., Nano-sized archaeota, with their small genomes and limited metabolic capabilities, are known to associate with other microbes, thereby compensating for their own auxotrophies. These diminutive and yet ubiquitous organisms thrive in hypersaline habitats that they share with haloarchaea. Here, we reveal the genetic and physiological nature of a nanohaloarchaeon–haloarchaeon association, with both microbes obtained from a solar saltern and reproducibly cultivated together in vitro. The nanohaloarchaeon Candidatus Nanohalobium constans LC1Nh is an aerotolerant, sugar-fermenting anaerobe, lacking key anabolic machinery and respiratory complexes. The nanohaloarchaeon cells are found physically connected to the chitinolytic haloarchaeon Halomicrobium sp. LC1Hm. Our experiments revealed that this haloarchaeon can hydrolyze chitin outside the cell (to produce the monosaccharide N-acetylglucosamine), using this beta-glucan to obtain carbon and energy for growth. However, LC1Hm could not metabolize either glycogen or starch (both alpha-glucans) or other polysaccharides tested. Remarkably, the nanohaloarchaeon’s ability to hydrolyze glycogen and starch to glucose enabled growth of Halomicrobium sp. LC1Hm in the absence of a chitin. These findings indicated that the nanohaloarchaeon–haloarchaeon association is both mutualistic and symbiotic; in this case, each microbe relies on its partner’s ability to degrade different polysaccharides. This suggests, in turn, that other nano-sized archaeota may also be beneficial for their hosts. Given that availability of carbon substrates can vary both spatially and temporarily, the susceptibility of Halomicrobium to colonization by Ca. Nanohalobium can be interpreted as a strategy to maximize the long-term fitness of the host., This study was partially supported by grants from the Italian Ministry of University and Research under the RITMARE Flagship Project (2012–2016) and the INMARE Project (Contract H2020-BG-2014-2634486), funded by the European Union’s Horizon 2020 Research Program. P.N.G. and O.V.G. acknowledge support from the Centre for Environmental Biotechnology Project, partly funded by the European Regional Development Fund via the Welsh Assembly Government. D.Y.S. was supported by SYAM-Gravitation Program of the Dutch Ministry of Education and Science Grant 24002002 and Russian Foundation for Basic Research Grant 19-04-00401). S.V.T. acknowledges Kurchatov Centre for Genome Research, and his work was supported by Ministry of Science and Higher Education of Russian Federation Grant 075-15-2019-1659.
Published: 2020

25. Reduced C9ORF72 function exacerbates gain of toxicity from ALS/FTD-causing repeat expansion in C9orf72

Author: Don W. Cleveland, Amy Taylor, Albert R. La Spada, Clotilde Lagier-Tourenne, Jie Jiang, Tania F. Gendron, Sandra Diaz Garcia, Huaxi Xu, John Ravits, Somasish Ghosh Dastidar, Lu-Lin Jiang, Leonard Petrucelli, Melissa McAlonis-Downes, María José Cubillas Rodríguez, Patrick King, Sandrine Da Cruz, Qiang Zhu, and Yong Jie Zhang
Subjects: 0301 basic medicine, Genetically modified mouse, General Neuroscience, Transgene, Autophagy, Endogeny, Biology, medicine.disease, Cell biology, C9orf72 Protein, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, C9orf72, medicine, Amyotrophic lateral sclerosis, Trinucleotide repeat expansion, Neuroscience, 030217 neurology & neurosurgery
Abstract: Hexanucleotide expansions in C9orf72, which encodes a predicted guanine exchange factor, are the most frequent genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Although repeat expansion has been established to generate toxic products, mRNAs encoding the C9ORF72 protein are also reduced in affected individuals. In this study, we tested how C9ORF72 protein levels affected repeat-mediated toxicity. In somatic transgenic mice expressing 66 GGGGCC repeats, inactivation of one or both endogenous C9orf72 alleles provoked or accelerated, respectively, early death. In mice expressing a C9orf72 transgene with 450 repeats that did not encode the C9ORF72 protein, inactivation of one or both endogenous C9orf72 alleles exacerbated cognitive deficits, hippocampal neuron loss, glial activation and accumulation of dipeptide-repeat proteins from translation of repeat-containing RNAs. Reduced C9ORF72 was shown to suppress repeat-mediated elevation in autophagy. These efforts support a disease mechanism in ALS/FTD resulting from reduced C9ORF72, which can lead to autophagy deficits, synergizing with repeat-dependent gain of toxicity.
Published: 2020

26. The Money Market Mutual Fund Liquidity Facility

Author: Kenechukwu Anadu, Marco Cipriani, Ryan Craver, and Gabriele La Spada
Subjects: History, Polymers and Plastics, Business and International Management, Industrial and Manufacturing Engineering
Published: 2022

27. Scarce, Abundant, or Ample? A Time-Varying Model of the Reserve Demand Curve

Author: Gara Afonso, Domenico Giannone, Gabriele La Spada, and John C. Williams
Subjects: History, Polymers and Plastics, Business and International Management, Industrial and Manufacturing Engineering
Published: 2022

28. Monetary Policy and the Run Risk of Loan Funds

Author: Nicola Cetorelli, Gabriele La Spada, and João A. C. Santos
Subjects: History, Polymers and Plastics, Business and International Management, Industrial and Manufacturing Engineering
Published: 2022

29. Banks’ Balance-Sheet Costs, Monetary Policy, and the ON RRP

Author: Gara Afonso, Marco Cipriani, and Gabriele La Spada
Subjects: History, Polymers and Plastics, Business and International Management, Industrial and Manufacturing Engineering
Published: 2022

30. La decisione del giudice di fronte all'alta conflittualità genitoriale: quando ricorrere alla coordinazione genitoriale

Author: Viviana La Spada, Monia Vagni, Claudia Rubis, Carlo Trionfi, Daniela Pajardi, and Stephanie Castoldi
Subjects: Health (social science), Social Psychology, Developmental and Educational Psychology
Abstract: Sempre più spesso le separazioni altamente conflittuali richiedono l'intervento del Tribunale per tutelare l'interesse dei minori. La letteratura internazionale, infatti, mostra come l'esposizione ad alti livelli di conflittualità genitoriale sia un fattore di rischio per i figli. Si propongono alcuni indicatori di conflittualità, rischio evolutivo e capacità di cura dei bisogni dei figli, come supporto, per il giudice e gli operatori, nella scelta degli interventi giudiziari e psicosociali più idonei. Si delineano vantaggi e finalità di interventi tradizionali (come la consulenza tecnica d'ufficio e la mediazione) e dell'innovativa pratica della coordinazione genitoriale.
Published: 2019

31. Depriving Mice of Sleep also Deprives of Food

Author: Nina Đukanović, Francesco La Spada, Yann Emmenegger, Guy Niederhäuser, Frédéric Preitner, and Paul Franken
Subjects: body composition, food intake, circadian rhythms, fat, digestive, oral, and skin physiology, energy expenditure, clock genes, lean body mass, sleep deprivation, General Earth and Planetary Sciences, General Environmental Science
Abstract: Both sleep-wake behavior and circadian rhythms are tightly coupled to energy metabolism and food intake. Altered feeding times in mice are known to entrain clock-gene rhythms in brain and liver and sleep-deprived humans tend to eat more and gain weight. Previous observations in mice showing that sleep deprivation (SD) changes clock-gene expression might thus relate to altered food intake and not to the loss of sleep per se. Whether SD affects food intake in the mouse and how this might affect clock-gene expression is, however, unknown. We therefore quantified i) the cortical expression of the clock genes Per1, Per2, Dbp, and Cry1 in mice that had access to food or not during a 6h SD, and ii) food intake during baseline, SD, and recovery sleep. We found that food deprivation did not modify the SD-incurred clock-gene changes in the cortex. Moreover, we discovered that although food intake during SD did not differ from baseline, mice lost weight and increased food intake during subsequent recovery. We conclude that SD is associated with food deprivation and that the resulting energy deficit might contribute to the effects of SD that are commonly interpreted as a response to sleep loss.
Published: 2021

32. De novo pathogenic variant in SETX causes a rapidly progressive neurodegenerative disorder of early childhood-onset with severe axonal polyneuropathy

Author: Aristides Hadjinicolaou, Kathie J. Ngo, Daniel Y. Conway, John P. Provias, Steven K. Baker, Lauren I. Brady, Craig L. Bennett, Albert R. La Spada, Brent L. Fogel, and Grace Yoon
Subjects: Male, Axonal neuropathy, Adolescent, DNA Helicases, SETX, Mice, Transgenic, Neurodegenerative Diseases, Case Report, Multifunctional Enzymes, Pathology and Forensic Medicine, Mice, Polyneuropathies, Cellular and Molecular Neuroscience, Animals, Humans, Neurology. Diseases of the nervous system, Neurology (clinical), Age of Onset, Neurodegeneration, RC346-429, Child, Senataxin, RNA Helicases
Abstract: Pathogenic variants in SETX cause two distinct neurological diseases, a loss-of-function recessive disorder, ataxia with oculomotor apraxia type 2 (AOA2), and a dominant gain-of-function motor neuron disorder, amyotrophic lateral sclerosis type 4 (ALS4). We identified two unrelated patients with the same de novo c.23C > T (p.Thr8Met) variant in SETX presenting with an early-onset, severe polyneuropathy. As rare private gene variation is often difficult to link to genetic neurological disease by DNA sequence alone, we used transcriptional network analysis to functionally validate these patients with severe de novo SETX-related neurodegenerative disorder. Weighted gene co-expression network analysis (WGCNA) was used to identify disease-associated modules from two different ALS4 mouse models and compared to confirmed ALS4 patient data to derive an ALS4-specific transcriptional signature. WGCNA of whole blood RNA-sequencing data from a patient with the p.Thr8Met SETX variant was compared to ALS4 and control patients to determine if this signature could be used to identify affected patients. WGCNA identified overlapping disease-associated modules in ALS4 mouse model data and ALS4 patient data. Mouse ALS4 disease-associated modules were not associated with AOA2 disease modules, confirming distinct disease-specific signatures. The expression profile of a patient carrying the c.23C > T (p.Thr8Met) variant was significantly associated with the human and mouse ALS4 signature, confirming the relationship between this SETX variant and disease. The similar clinical presentations of the two unrelated patients with the same de novo p.Thr8Met variant and the functional data provide strong evidence that the p.Thr8Met variant is pathogenic. The distinct phenotype expands the clinical spectrum of SETX-related disorders.
Published: 2021

33. MAP4K3 inhibits Sirtuin-1 to repress the LKB1-AMPK pathway to promote amino acid dependent activation of the mTORC1 complex

Author: Cynthia Hsu, J. Paul Taylor, Kohta Ohnishi, Bryce L. Sopher, Tony Hunter, Mary Rose Branch, Elian Lee, Albert R. La Spada, Jill Meisenhelder, and Brett J. Winborn
Subjects: chemistry.chemical_classification, biology, Sirtuin 1, Effector, AMPK, mTORC1, Cell biology, Amino acid, chemistry, biology.protein, Phosphorylation, biological phenomena, cell phenomena, and immunity, Signal transduction, RHEB
Abstract: mTORC1 is the key rheostat controlling cellular metabolic state. Of the various inputs to mTORC1, the most potent effector of intracellular nutrient status is amino acid supply. Despite an established role for MAP4K3 in promoting mTORC1 activation in the presence of amino acids, the signaling pathway by which MAP4K3 controls mTORC1 activation remains unknown. Here we examined the process of MAP4K3 activation of mTORC1 and found that MAP4K3 represses the LKB1-AMPK pathway to prevent TSC1/2 complex inactivation of Rheb. When we sought the regulatory link between MAP4K3 and LKB1 inhibition, we discovered that MAP4K3 physically interacts with the master nutrient regulatory factor Sirtuin-1 and phosphorylates Sirtuin-1 to repress LKB1 activation. Our results reveal the existence of a novel signaling pathway linking amino acid satiety with MAP4K3-dependent suppression of SIRT1 to inactivate the repressive LKB1-AMPK pathway and thereby potently activate the mTORC1 complex to dictate the metabolic disposition of the cell.
Published: 2021

34. Longitudinal investigation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in older patients in the province of Palermo (Southern Italy) during the early wave of the pandemic

Author: Alessandro Scorsone, Paola Di Carlo, Dario De Luca, Laura Maniscalco, Emanuele La Spada, Marco Enea, Domenica Matranga, Davide Brancato, Domenica MATRANGA, Laura Maniscalco, Marco Enea, Dario De Luca, Davide Brancato, Emanuele La Spada, Alessandro Scorsone, and Paola Di Carlo
Subjects: medicine.medical_specialty, business.industry, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), General Medicine, chronic kidney failure, medicine.disease, Settore MED/01 - Statistica Medica, Chronic kidney failure, Older patients, diabete, Internal medicine, Diabetes mellitus, D-dimer, Pandemic, Medicine, Dementia, Neutrophils/Lymphocytes Ratio, business, prognostic factor, dementia
Abstract: IntroductionClinical presentation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in old adults from Southern Italy is little known. This study aims to investigate the mortality risk related to risk factors, therapy and clinical course and to suggest prognostic indicators based on day-to-day follow-up of clinical and laboratory findings.Material and methodsIt was designed as a retrospective longitudinal cohort study of adult SARS-CoV-2 patients admitted at Partinico COVID Hospital in Palermo, Southern Italy. Patients were recruited between 4 March and 25 April and followed up until 31 May 2020, day-to-day until death or hospital discharge. Clinical data, laboratory tests and treatment data were extracted from medical records and epidemiologic information was obtained by clinical history and the medical interview.ResultsForty-seven patients (median age = 75 IQR: 59.50–86.00) were followed up during a 87 days observation period, accounting for a total of 1,035 person days. At the end of follow-up, 28 (60%) patients were discharged and 19 (40%) died, so that the estimated incidence density rate was 0.018 deaths per day (18 SARS-CoV-2-related deaths per 1,000 patient days). Diabetes (HR = 8.13, 95% CI: 1.91–34.67), chronic kidney failure (HR = 5.86, 95% CI: 1.36–25.21), dementia (HR = 7.84, 95% CI: 1.80–34.20), and neutrophil/lymphocyte ratio > 7 (HR = 10.37, 95% CI: 2.24–48.14) were found as significant prognostic factors.ConclusionsThe joint evaluation of dementia, diabetes, chronic kidney failure and neutrophil/lymphocyte ratio showed an optimal prognostic value already in the first week of follow-up. The day-to-day follow-up provides essential information for clinical monitoring and treatment of the disease in a hospital setting and improves the disease’s home management, especially for older patients with frailty.
Published: 2020

35. Clonally expanded CD8 T cells characterize Amyotrophic Lateral Sclerosis 4

Author: Cindy Beharry, Jessica Sook Yuin Ho, Frederick Arnold, Lorena Mosca, Anastasia Gromova, Lyle Ostrow, Laura Campisi, Ivan Marazzi, Neil A. Shneider, Shahab Chizari, Xueyan Mei, Yesai Fstkchyan, Ning Jiang, Christian Lunetta, Albert R. La Spada, Jack Prazich, Craig L. Bennett, and Vlad Korobeynikov
Subjects: Pathology, medicine.medical_specialty, medicine, Cytotoxic T cell, Amyotrophic lateral sclerosis, Biology, medicine.disease
Abstract: Amyotrophic Lateral Sclerosis (ALS) is a heterogeneous neurodegenerative disorder that affects motor neurons in the brain and spinal cord, causing progressive loss of voluntary muscle control1,2. ALS heterogeneity includes the age of manifestation, the rate of progression, and the anatomical sites of symptom onset. In addition, disease-causing mutations in specific genes have been identified and are used to catalog different subtypes of ALS3. Interestingly, several ALS-associated genes have been shown to affect immune functions, and a variety of aberrant inflammatory events have been reported in patients and mouse models4-11, suggesting that specific immune features can also account for ALS heterogeneity. ALS4 is characterized by juvenile-onset and slow progression12. After experiencing mild symptoms during their childhood, ALS4 patients show motor difficulties by their 30s, and most of them require walkers or wheelchairs by their 50s. ALS4 is caused by dominant mutations in the gene SETX. Using Setx knock-in (KI) mice carrying the ALS4 causative L389S mutation, we discovered an immunological signature consisting of clonally activated CD8 T cells specifically in the central nervous system and blood of KI animals. Expansion of antigen-specific CD8 T cells mirrors disease progression. Bone marrow transplantation experiments indicate an essential role of the immune system in ALS4 neurodegeneration. Furthermore, we found that clonally expanded CD8 T cells circulate in the peripheral blood of ALS4 patients. Our results provide evidence of an antigen-specific CD8 T cell response linked to ALS4, and can serve not only to unravel specific disease mechanisms, but as a potential biomarker of disease activity.
Published: 2021

36. Author Correction: Clonally expanded CD8 T cells characterize amyotrophic lateral sclerosis-4

Author: Laura Campisi, Shahab Chizari, Jessica S. Y. Ho, Anastasia Gromova, Frederick J. Arnold, Lorena Mosca, Xueyan Mei, Yesai Fstkchyan, Denis Torre, Cindy Beharry, Marta Garcia-Forn, Miguel Jiménez-Alcázar, Vladislav A. Korobeynikov, Jack Prazich, Zahi A. Fayad, Marcus M. Seldin, Silvia De Rubeis, Craig L. Bennett, Lyle W. Ostrow, Christian Lunetta, Massimo Squatrito, Minji Byun, Neil A. Shneider, Ning Jiang, Albert R. La Spada, and Ivan Marazzi
Subjects: Multidisciplinary
Published: 2022

37. TFEB dysregulation as a driver of autophagy dysfunction in neurodegenerative disease: Molecular mechanisms, cellular processes, and emerging therapeutic opportunities

Author: Albert R. La Spada and Constanza J. Cortes
Subjects: 0301 basic medicine, Parkinson's disease, Transcription factor EB, Article, lcsh:RC321-571, 03 medical and health sciences, 0302 clinical medicine, Huntington's disease, Lysosome, Autophagy, Animals, Humans, Medicine, Neurodegeneration, Amyotrophic lateral sclerosis, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, business.industry, Neurodegenerative Diseases, Alzheimer's disease, medicine.disease, 030104 developmental biology, Proteostasis, medicine.anatomical_structure, Neurology, TFEB, business, Neuroscience, 030217 neurology & neurosurgery
Abstract: Two decades ago, the recognition of protein misfolding and aggregate accumulation as defining features of neurodegenerative disease set the stage for a thorough examination of how protein quality control is maintained in neurons and in other non-neuronal cells in the central nervous system (CNS). Autophagy, a pathway of cellular self-digestion, has emerged as especially important for CNS proteostasis, and autophagy dysregulation has been documented as a defining feature of neurodegeneration in Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). Transcription factor EB (TFEB) is one of the main transcriptional regulators of autophagy, as it promotes the expression of genes required for autophagosome formation, lysosome biogenesis, and lysosome function, and it is highly expressed in CNS. Over the last 7 years, TFEB has received considerable attention and TFEB dysfunction has been implicated in the pathogenesis of numerous neurodegenerative disorders. In this review, we delineate the current understanding of how TFEB dysregulation is involved in neurodegeneration, highlighting work done on AD, PD, HD, X-linked spinal & bulbar muscular atrophy, and amyotrophic lateral sclerosis. Because TFEB is a central node in defining autophagy activation status, efforts at understanding the basis for TFEB dysfunction are yielding insights into how TFEB might be targeted for therapeutic application, which may represent an exciting opportunity for the development of a treatment modality with broad application to neurodegeneration.
Published: 2019

38. Stress e competenze genitoriali nelle separazioni giudiziarie. Analisi dei fattori protettivi e di rischio nelle relazioni parentali

Author: Viviana La Spada, Daniela Pajardi, Valeria Giostra, Tiziana Maiorano, and Monia Vagni
Subjects: Expert witness, media_common.quotation_subject, Scale (social sciences), Stress (linguistics), Context (language use), Psychology, Affect (psychology), Psychological abuse, General Psychology, Prejudice (legal term), Neglect, media_common, Developmental psychology
Abstract: Parental stress is a psycho-social dimension of the parent-child relationship and is influenced by the context in which the relationship is experienced. Separa-tion can affect the functionality/dysfunctionality of parenting skills and the level and quality of perceived stress. The main goal of the present study is to investiga-te the possible predictive effect of parental stress perceived during judicial sepa-ration on parental behaviors of risk and/or psychological prejudice. On a sample of 22 parental couples involved in psychological expert witness, the PSI (Paren-ting Stress Index; Abidin, 1986) was administered in order to analyze parental stress level that takes into account the representation that the parent has of his/her child and of the relationship with him/her. The results reported in the PSI will be analyzed in relation to the evaluation of parental skills conducted with the APS-I tool (Assessment of Parental Skills Interview; Camerini et al., 2007). The results show how high parental stress, especially when perceived in the relation-ship with the child (PCDI scale), tends to assume a predictive effect of risk of emotional abuse and/or emotional and psychological neglect. Parental stress can be an interesting key to understanding dynamics between parents and children and parenting skills, useful both from a clinical point of view and in expert wit-ness in court.
Published: 2019

39. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1

Author: Klionsky, Daniel J, Abdel-Aziz, Amal Kamal, Abdelfatah, Sara, Abdellatif, Mahmoud, Abdoli, Asghar, Abel, Steffen, Abeliovich, Hagai, Abildgaard, Marie H, Abudu, Yakubu Princely, Acevedo-Arozena, Abraham, Adamopoulos, Iannis E, Adeli, Khosrow, Adolph, Timon E, Adornetto, Annagrazia, Aflaki, Elma, Agam, Galila, Agarwal, Anupam, Aggarwal, Bharat B, Agnello, Maria, Agostinis, Patrizia, Agrewala, Javed N, Agrotis, Alexander, Aguilar, Patricia V, Ahmad, S Tariq, Ahmed, Zubair M, Ahumada-Castro, Ulises, Aits, Sonja, Aizawa, Shu, Akkoc, Yunus, Akoumianaki, Tonia, Akpinar, Hafize Aysin, Al-Abd, Ahmed M, Al-Akra, Lina, Al-Gharaibeh, Abeer, Alaoui-Jamali, Moulay A, Alberti, Simon, Alcocer-Gómez, Elísabet, Alessandri, Cristiano, Ali, Muhammad, Alim Al-Bari, M Abdul, Aliwaini, Saeb, Alizadeh, Javad, Almacellas, Eugènia, Almasan, Alexandru, Alonso, Alicia, Alonso, Guillermo D, Altan-Bonnet, Nihal, Altieri, Dario C, Álvarez, Élida MC, Alves, Sara, Alves Da Costa, Cristine, Alzaharna, Mazen M, Amadio, Marialaura, Amantini, Consuelo, Amaral, Cristina, Ambrosio, Susanna, Amer, Amal O, Ammanathan, Veena, An, Zhenyi, Andersen, Stig U, Andrabi, Shaida A, Andrade-Silva, Magaiver, Andres, Allen M, Angelini, Sabrina, Ann, David, Anozie, Uche C, Ansari, Mohammad Y, Antas, Pedro, Antebi, Adam, Antón, Zuriñe, Anwar, Tahira, Apetoh, Lionel, Apostolova, Nadezda, Araki, Toshiyuki, Araki, Yasuhiro, Arasaki, Kohei, Araújo, Wagner L, Araya, Jun, Arden, Catherine, Arévalo, Maria-Angeles, Arguelles, Sandro, Arias, Esperanza, Arikkath, Jyothi, Arimoto, Hirokazu, Ariosa, Aileen R, Armstrong-James, Darius, Arnauné-Pelloquin, Laetitia, Aroca, Angeles, Arroyo, Daniela S, Arsov, Ivica, Artero, Rubén, Asaro, Dalia Maria Lucia, Aschner, Michael, Ashrafizadeh, Milad, Ashur-Fabian, Osnat, Atanasov, Atanas G, Au, Alicia K, Auberger, Patrick, Auner, Holger W, Aurelian, Laure, Autelli, Riccardo, Avagliano, Laura, Ávalos, Yenniffer, Aveic, Sanja, Aveleira, Célia Alexandra, Avin-Wittenberg, Tamar, Aydin, Yucel, Ayton, Scott, Ayyadevara, Srinivas, Azzopardi, Maria, Baba, Misuzu, Backer, Jonathan M, Backues, Steven K, Bae, Dong-Hun, Bae, Ok-Nam, Bae, Soo Han, Baehrecke, Eric H, Baek, Ahruem, Baek, Seung-Hoon, Baek, Sung Hee, Bagetta, Giacinto, Bagniewska-Zadworna, Agnieszka, Bai, Hua, Bai, Jie, Bai, Xiyuan, Bai, Yidong, Bairagi, Nandadulal, Baksi, Shounak, Balbi, Teresa, Baldari, Cosima T, Balduini, Walter, Ballabio, Andrea, Ballester, Maria, Balazadeh, Salma, Balzan, Rena, Bandopadhyay, Rina, Banerjee, Sreeparna, Banerjee, Sulagna, Bánréti, Ágnes, Bao, Yan, Baptista, Mauricio S, Baracca, Alessandra, Barbati, Cristiana, Bargiela, Ariadna, Barilà, Daniela, Barlow, Peter G, Barmada, Sami J, Barreiro, Esther, Barreto, George E, Bartek, Jiri, Bartel, Bonnie, Bartolome, Alberto, Barve, Gaurav R, Basagoudanavar, Suresh H, Bassham, Diane C, Bast, Robert C, Basu, Alakananda, Batoko, Henri, Batten, Isabella, Baulieu, Etienne E, Baumgarner, Bradley L, Bayry, Jagadeesh, Beale, Rupert, Beau, Isabelle, Beaumatin, Florian, Bechara, Luiz RG, Beck, George R, Beers, Michael F, Begun, Jakob, Behrends, Christian, Behrens, Georg MN, Bei, Roberto, Bejarano, Eloy, Bel, Shai, Behl, Christian, Belaid, Amine, Belgareh-Touzé, Naïma, Bellarosa, Cristina, Belleudi, Francesca, Belló Pérez, Melissa, Bello-Morales, Raquel, Beltran, Jackeline Soares De Oliveira, Beltran, Sebastián, Benbrook, Doris Mangiaracina, Bendorius, Mykolas, Benitez, Bruno A, Benito-Cuesta, Irene, Bensalem, Julien, Berchtold, Martin W, Berezowska, Sabina, Bergamaschi, Daniele, Bergami, Matteo, Bergmann, Andreas, Berliocchi, Laura, Berlioz-Torrent, Clarisse, Bernard, Amélie, Berthoux, Lionel, Besirli, Cagri G, Besteiro, Sebastien, Betin, Virginie M, Beyaert, Rudi, Bezbradica, Jelena S, Bhaskar, Kiran, Bhatia-Kissova, Ingrid, Bhattacharya, Resham, Bhattacharya, Sujoy, Bhattacharyya, Shalmoli, Bhuiyan, Md Shenuarin, Bhutia, Sujit Kumar, Bi, Lanrong, Bi, Xiaolin, Biden, Trevor J, Bijian, Krikor, Billes, Viktor A, Binart, Nadine, Bincoletto, Claudia, Birgisdottir, Asa B, Bjorkoy, Geir, Blanco, Gonzalo, Blas-Garcia, Ana, Blasiak, Janusz, Blomgran, Robert, Blomgren, Klas, Blum, Janice S, Boada-Romero, Emilio, Boban, Mirta, Boesze-Battaglia, Kathleen, Boeuf, Philippe, Boland, Barry, Bomont, Pascale, Bonaldo, Paolo, Bonam, Srinivasa Reddy, Bonfili, Laura, Bonifacino, Juan S, Boone, Brian A, Bootman, Martin D, Bordi, Matteo, Borner, Christoph, Bornhauser, Beat C, Borthakur, Gautam, Bosch, Jürgen, Bose, Santanu, Botana, Luis M, Botas, Juan, Boulanger, Chantal M, Boulton, Michael E, Bourdenx, Mathieu, Bourgeois, Benjamin, Bourke, Nollaig M, Bousquet, Guilhem, Boya, Patricia, Bozhkov, Peter V, Bozi, Luiz HM, Bozkurt, Tolga O, Brackney, Doug E, Brandts, Christian H, Braun, Ralf J, Braus, Gerhard H, Bravo-Sagua, Roberto, Bravo-San Pedro, José M, Brest, Patrick, Bringer, Marie-Agnès, Briones-Herrera, Alfredo, Broaddus, V Courtney, Brodersen, Peter, Brodsky, Jeffrey L, Brody, Steven L, Bronson, Paola G, Bronstein, Jeff M, Brown, Carolyn N, Brown, Rhoderick E, Brum, Patricia C, Brumell, John H, Brunetti-Pierri, Nicola, Bruno, Daniele, Bryson-Richardson, Robert J, Bucci, Cecilia, Buchrieser, Carmen, Bueno, Marta, Buitrago-Molina, Laura Elisa, Buraschi, Simone, Buch, Shilpa, Buchan, J Ross, Buckingham, Erin M, Budak, Hikmet, Budini, Mauricio, Bultynck, Geert, Burada, Florin, Burgoyne, Joseph R, Burón, M Isabel, Bustos, Victor, Büttner, Sabrina, Butturini, Elena, Byrd, Aaron, Cabas, Isabel, Cabrera-Benitez, Sandra, Cadwell, Ken, Cai, Jingjing, Cai, Lu, Cai, Qian, Cairó, Montserrat, Calbet, Jose A, Caldwell, Guy A, Caldwell, Kim A, Call, Jarrod A, Calvani, Riccardo, Calvo, Ana C, Calvo-Rubio Barrera, Miguel, Camara, Niels Os, Camonis, Jacques H, Camougrand, Nadine, Campanella, Michelangelo, Campbell, Edward M, Campbell-Valois, François-Xavier, Campello, Silvia, Campesi, Ilaria, Campos, Juliane C, Camuzard, Olivier, Cancino, Jorge, Candido De Almeida, Danilo, Canesi, Laura, Caniggia, Isabella, 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Zhang, Yuchen, Zhang, Zhe, Zhang, Zhengguang, Zhang, Zhibing, Zhang, Zhihai, Zhang, Zhiyong, Zhang, Zili, Zhao, Haobin, Zhao, Lei, Zhao, Shuang, Zhao, Tongbiao, Zhao, Xiao-Fan, Zhao, Ying, Zhao, Yongchao, Zhao, Yongliang, Zhao, Yuting, Zheng, Guoping, Zheng, Kai, Zheng, Ling, Zheng, Shizhong, Zheng, Xi-Long, Zheng, Yi, Zheng, Zu-Guo, Zhivotovsky, Boris, Zhong, Qing, Zhou, Ao, Zhou, Ben, Zhou, Cefan, Zhou, Gang, Zhou, Hao, Zhou, Hong, Zhou, Hongbo, Zhou, Jie, Zhou, Jing, Zhou, Jiyong, Zhou, Kailiang, Zhou, Rongjia, Zhou, Xu-Jie, Zhou, Yanshuang, Zhou, Yinghong, Zhou, Yubin, Zhou, Zheng-Yu, Zhou, Zhou, Zhu, Binglin, Zhu, Changlian, Zhu, Guo-Qing, Zhu, Haining, Zhu, Hongxin, Zhu, Hua, Zhu, Wei-Guo, Zhu, Yanping, Zhu, Yushan, Zhuang, Haixia, Zhuang, Xiaohong, Zientara-Rytter, Katarzyna, Zimmermann, Christine M, Ziviani, Elena, Zoladek, Teresa, Zong, Wei-Xing, Zorov, Dmitry B, Zorzano, Antonio, Zou, Weiping, Zou, Zhen, Zou, Zhengzhi, Zuryn, Steven, Zwerschke, Werner, Brand-Saberi, Beate, Dong, X Charlie, Kenchappa, Chandra Shekar, Li, Zuguo, Lin, Yong, Oshima, Shigeru, Rong, Yueguang, Sluimer, Judith C, Stallings, Christina L, and Tong, Chun-Kit
Subjects: phagophore, vacuole, Autophagosome, neurodegeneration, Autophagosomes, Autophagy-Related Proteins, flux, macroautophagy, stress, LC3, lysosome, Autophagy, cancer, Animals, Humans, Biological Assay, Lysosomes, Biomarkers
Abstract: In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Published: 2021
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40. Natural Biostimulants Elicit Plant Immune System in an Integrated Management Strategy of the Postharvest Green Mold of Orange Fruits Incited by

Author: Federico, La Spada, Francesco, Aloi, Maurizio, Coniglione, Antonella, Pane, and Santa Olga, Cacciola
Subjects: biostimulants, resistance genes, fungicide residues, food and beverages, algal and plant extracts, Plant Science, imazalil, resistance-inducers, Original Research, Citrus sinensis
Abstract: This study was aimed at testing the integrated use of a natural biostimulant based on seaweed (Ascophyllum nodosum) and plant (alfalfa and sugarcane) extracts and reduced dosages of the conventional synthetic fungicide Imazalil (IMZ) to manage postharvest rots of orange fruits. The following aspects were investigated: (i) the effectiveness of postharvest treatment with natural biostimulant alone or in mixture with IMZ at a reduced dose against green mold caused by Penicillium digitatum; (ii) the differential expression of defense genes in orange fruits treated with the natural biostimulant both alone and in combination with a reduced dose of IMZ; (iii) the persistence of the inhibitory activity of both biostimulant and the mixture biostimulant/IMZ against green mold; and (iv) the residue level of fungicide in citrus peel when applied alone or in combination with the biostimulant. Treatments with the chemical plant resistance-inducer potassium phosphite, alone or with a reduced dose of IMZ, were included for comparison. The mixture of natural biostimulant and IMZ at a low dose consistently reduced the incidence and severity of fruit green mold and induced a significant increase of the expression level of β-1,3-glucanase-, peroxidase (PEROX)-, and phenylalanine ammonia-lyase (PAL)-encoding genes in fruit peel, suggesting that the natural biostimulant elicits a long-lasting resistance of citrus fruits to infections by P. digitatum. Interestingly, the residual concentration of IMZ in fruits treated with the biostimulant/fungicide mixture was significantly lower than that of IMZ in fruits treated only with the fungicide at the same dose and by far below the threshold values set by the European Union. This study laid the foundations for (i) conceiving a practical and more eco-friendly alternative to the conventional postharvest management of green mold of citrus fruits, based almost exclusively on the use of synthetic fungicide IMZ, alone or mixed with potassium phosphite and (ii) providing a better insight into the mechanisms of disease resistance induction by biostimulants.
Published: 2021

41. Author response: Miniaturized 3D bone marrow tissue model to assess response to Thrombopoietin-receptor agonists in patients

Author: Hana Raslova, Carlo Zaninetti, Christian A. Di Buduo, James B. Bussel, Aikaterini Ntai, Pierre-Alexandre Laurent, Alessandra Balduini, Alessandro Pecci, Ida Biunno, Serena Barozzi, David L. Kaplan, Carlo L. Balduini, Alberto La Spada, Paolo M. Soprano, and Larissa Lordier
Subjects: Thrombopoietin Receptor Agonists, medicine.anatomical_structure, business.industry, Tissue Model, Cancer research, medicine, In patient, Bone marrow, business
Published: 2021

42. Inhibitory effect of plant extracts on the cytotoxicity of eurytele nematocysts from Pelagia noctiluca

Author: Gian Luigi Mariottini, Angela Marino, Bruno Burlando, Giuseppina La Spada, Alessia Remigante, Laura Cornara, and Rossana Morabito
Subjects: Biochemistry, Biochemistry (medical), Plant Science, Cnidocyte, Biology, Cytotoxicity, Pelagia noctiluca, biology.organism_classification, Inhibitory effect, General Biochemistry, Genetics and Molecular Biology
Abstract: Some species of Cnidarians, well known venomous organisms, are able to induce serious health problems as well as economic and social trouble. A lot of data show that cnidarian venoms can be cytotoxic to cultured cells. Therefore, a priority of the research is to find tools which could counteract the damaging activity of venoms. In this connection, the modulatory effects exerted by extracts of plants Ananas comosus (L.) and Carica papaya (L.) on cytotoxicity of heterotrichous microbasic eurytele nematocysts isolated from the jellyfish Pelagia noctiluca was evaluated. The nematocyst extract induced strong cytotoxicity at highest tested doses with reduction of cell survival below 40% and IC50 value of 40×103 nematocysts/mL. Both plant extracts significantly improved the survival of cells, so that the IC50 resulted 74×103 and 100×103 nematocysts/mL in the presence of A. comosus and C. papaya extracts, respectively, both used at 10 and 100 μg/mL. Taking into account that heterotrichous microbasic eurytele nematocysts are present mainly in tentacles, which Pelagia noctiluca utilizes both for predation and defence, this result is particularly interesting from both ecological and sanitary point of view and demonstrates the potential of these plants extracts against cnidarian venoms.
Published: 2021

43. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

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B, Zhou, CF, Zhou, G, Zhou, H, Zhou, HB, Zhou, J, Zhou, JY, Zhou, KL, Zhou, RJ, Zhou, XJ, Zhou, YS, Zhou, YH, Zhou, YB, Zhou, ZY, Zhou, Z, Zhu, BL, Zhu, CL, Zhu, GQ, Zhu, HN, Zhu, HX, Zhu, H, Zhu, WG, Zhu, YP, Zhu, YS, Zhuang, HX, Zhuang, XH, Zientara-Rytter, K, Zimmermann, CM, Ziviani, E, Zoladek, T, Zong, WX, Zorov, DB, Zorzano, A, Zou, WP, Zou, Z, Zou, ZZ, Zuryn, S, Zwerschke, W, Brand-Saberi, B, Dong, XC, Kenchappa, CS, Li, ZG, Lin, Y, Oshima, S, Rong, YG, Sluimer, JC, Stallings, CL, and Tong, CK
Subjects: flux, macroautophagy, phagophore, stress, vacuole, Autophagosome, LC3, lysosome, neurodegeneration, cancer
Abstract: In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Published: 2021

44. Huntingtin Maintains Mitochondrial Genome Integrity and Function

Author: Leslie M. Thompson, Narattam Sikdar, Rui Gao, Nan Zhang, Subrata Pradhan, Tetsuo Ashizawa, Albert R. La Spada, Sanjeev Choudhary, Keegan M. Bush, Audrey S. Dickey, Tapas K. Hazra, Yogesh P. Wairkar, Partha S. Sarkar, C. Dirk Keene, Subo Yuan, Lisa M. Ellerby, Charlene Smith-Geater, Eva L. Morozko, Jeffrey Snowden, and Anirban Chakraborty
Subjects: chemistry.chemical_compound, Mitochondrial DNA, Huntingtin, chemistry, biology, DNA repair, Transcription (biology), biology.protein, Mitochondrion, Transcription factor, DNA, Polymerase, Cell biology
Abstract: SUMMARYThe function of huntingtin (HTT) is enigmatic in that the native protein provides neuroprotection while mutant HTT (mHTT) carrying an expanded stretch of glutamines triggers neurotoxicity in Huntington’s disease (HD). We recently reported that HTT forms a transcription-coupled DNA repair (TCR) complex with RNA polymerase and DNA repair enzyme polynucleotide-kinase-3'-phosphatase (PNKP). This complex resolves DNA lesions during transcription to maintain genome integrity, while mHTT impairs the activity of this complex, resulting in DNA lesion accumulation, activating the DNA damage-response in HD. Here we report that HTT forms a DNA repair complex within the mitochondria with mitochondrial RNA polymerase, transcription factors, and PNKP. This complex resolves mitochondrial DNA (mtDNA) lesions to preserve mtDNA integrity and function. Pathogenic mHTT reduces the complex activity, resulting in persistence of mtDNA lesions, impairing mitochondrial function in HD. Restoring the activity of the mtDNA repair complex in a Drosophila model of HD dramatically improves mtDNA integrity, and motor defects.
Published: 2021

45. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Author: D. KLIONSKY, A. ABDEL-AZIZ, S. ABDELFATAH, M. ABDELLATIF, A. ABDOLI, S. ABEL, H. ABELIOVICH, M. ABILDGAARD, Y. ABUDU, A. ACEVEDO-AROZENA, I. ADAMOPOULOS, K. ADELI, T. ADOLPH, A. ADORNETTO, E. AFLAKI, G. AGAM, A. AGARWAL, B. AGGARWAL, M. AGNELLO, P. AGOSTINIS, J. AGREWALA, A. AGROTIS, P. AGUILAR, S. AHMAD, Z. AHMED, U. AHUMADA-CASTRO, S. AITS, S. AIZAWA, Y. AKKOC, T. AKOUMIANAKI, H. AKPINAR, A. AL-ABD, L. AL-AKRA, A. AL-GHARAIBEH, M. ALAOUI-JAMALI, S. ALBERTI, E. ALCOCER-GOMEZ, C. ALESSANDRI, M. ALI, M. AL-BARI, S. ALIWAINI, J. ALIZADEH, E. ALMACELLAS, A. ALMASAN, A. ALONSO, G. ALONSO, N. ALTAN-BONNET, D. ALTIERI, S. ALVES, C. DA COSTA, M. ALZAHARNA, M. AMADIO, C. AMANTINI, C. AMARAL, S. AMBROSIO, A. AMER, V. AMMANATHAN, Z. AN, S. ANDERSEN, S. ANDRABI, M. ANDRADE-SILVA, A. ANDRES, S. ANGELINI, D. ANN, U. ANOZIE, M. ANSARI, P. ANTAS, A. ANTEBI, Z. ANTON, T. ANWAR, L. APETOH, N. APOSTOLOVA, T. ARAKI, Y. ARAKI, K. ARASAKI, W. ARAUJO, J. ARAYA, C. ARDEN, M. AREVALO, S. ARGUELLES, E. ARIAS, J. ARIKKATH, H. ARIMOTO, A. ARIOSA, D. ARMSTRONG-JAMES, L. ARNAUNE-PELLOQUIN, A. AROCA, D. ARROYO, I. ARSOV, R. ARTERO, D. ASARO, M. ASCHNER, M. ASHRAFIZADEH, O. ASHUR-FABIAN, A. ATANASOV, A. AU, P. AUBERGER, H. AUNER, L. AURELIAN, R. AUTELLI, L. AVAGLIANO, Y. AVALOS, S. AVEIC, C. AVELEIRA, T. AVINWITTENBERG, Y. AYDIN, S. AYTON, S. AYYADEVARA, M. AZZOPARDI, M. BABA, J. BACKER, S. BACKUES, D. BAE, O. BAE, S. BAE, E. BAEHRECKE, A. BAEK, S. BAEK, G. BAGETTA, A. BAGNIEWSKA-ZADWORNA, H. BAI, J. BAI, X. BAI, Y. BAI, N. BAIRAGI, S. BAKSI, T. BALBI, C. BALDARI, W. BALDUINI, A. BALLABIO, M. BALLESTER, S. BALAZADEH, R. BALZAN, R. BANDOPADHYAY, S. BANERJEE, Y. BAO, M. BAPTISTA, A. BARACCA, C. BARBATI, A. BARGIELA, D. BARILA, P. BARLOW, S. BARMADA, E. BARREIRO, G. BARRETO, J. BARTEK, B. BARTEL, A. BARTOLOME, G. BARVE, S. BASAGOUDANAVAR, D. BASSHAM, R. JR, A. BASU, H. BATOKO, I. BATTEN, E. BAULIEU, B. BAUMGARNER, J. BAYRY, R. BEALE, I. BEAU, F. BEAUMATIN, L. BECHARA, G. 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CRACK, J. CRESPO, A. CRIOLLO, V. CRIPPA, R. CRISTOFANI, T. CSIZMADIA, A. CUADRADO, B. CUI, J. CUI, Y. CUI, E. CULETTO, A. CUMINO, A. CYBULSKY, M. CZAJA, S. CZUCZWAR, S. D'ADAMO, M. D'AMELIO, D. D'ARCANGELO, A. D'LUGOS, G. D'ORAZI, J. DA SILVA, H. DAFSARI, R. DAGDA, Y. DAGDAS, M. DAGLIA, X. DAI, Y. DAI, J. DAL COL, P. DALHAIMER, L. DALLA VALLE, T. DALLENGA, G. DALMASSO, M. DAMME, I. DANDO, N. DANTUMA, A. DARLING, H. DAS, S. DASARATHY, S. DASARI, S. DASH, O. DAUMKE, A. DAUPHINEE, J. DAVIES, V. DAVILA, R. DAVIS, T. DAVIS, S. NAIDU, F. DE AMICIS, K. DE BOSSCHER, F. DE FELICE, L. DE FRANCESCHI, C. DE LEONIBUS, M. BARBOSA, G. DE MEYER, A. DE MILITO, C. DE NUNZIO, C. DE PALMA, M. DE SANTI, C. DE VIRGILIO, D. DE ZIO, J. DEBNATH, B. DEBOSCH, J. DECUYPERE, M. DEEHAN, G. DEFLORIAN, J. DEGREGORI, B. DEHAY, G. DEL RIO, J. DELANEY, L. DELBRIDGE, E. DELORME-AXFORD, M. DELPINO, F. DEMARCHI, V. DEMBITZ, N. DEMERS, H. DENG, Z. DENG, J. DENGJEL, P. DENT, D. DENTON, M. DEPAMPHILIS, C. DER, V. DERETIC, A. DESCOTEAUX, L. DEVIS, S. DEVKOTA, O. DEVUYST, G. DEWSON, M. DHARMASIVAM, R. DHIMAN, D. DI BERNARDO, M. DI CRISTINA, F. DI DOMENICO, P. DI FAZIO, A. DI FONZO, G. DI GUARDO, G. DI GUGLIELMO, L. DI LEO, C. DI MALTA, A. DI NARDO, M. DI RIENZO, F. DI SANO, G. DIALLINAS, J. DIAO, G. DIAZ-ARAYA, I. DIAZ-LAVIADA, J. DICKINSON, M. DIEDERICH, M. DIEUDE, I. DIKIC, S. DING, W. DING, L. DINI, M. DINIC, A. DINKOVA-KOSTOVA, M. DIONNE, J. DISTLER, A. DIWAN, I. DIXON, M. DJAVAHERI-MERGNY, I. DOBRINSKI, O. DOBROVINSKAYA, R. DOBROWOLSKI, R. DOBSON, S. EMRE, M. DONADELLI, B. DONG, X. DONG, Z. DONG, G. II, V. DOTSCH, H. DOU, J. DOU, M. DOWAIDAR, S. DRIDI, L. DRUCKER, A. DU, C. DU, G. DU, H. DU, L. DU, A. DU TOIT, S. DUAN, X. DUAN, S. DUARTE, A. DUBROVSKA, E. DUNLOP, N. DUPONT, R. DURAN, B. DWARAKANATH, S. DYSHLOVOY, D. EBRAHIMI-FAKHARI, L. ECKHART, C. EDELSTEIN, T. EFFERTH, E. EFTEKHARPOUR, L. EICHINGER, N. EID, T. EISENBERG, N. EISSA, S. EISSA, M. EJARQUE, A. EL ANDALOUSSI, N. EL-HAGE, S. EL-NAGGAR, A. 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REN, T. RENAULT, G. RENGA, K. REUE, K. REWITZ, B. RAMOS, S. RIAZUDDIN, T. RIBEIRO-RODRIGUES, J. RICCI, R. RICCI, V. RICCIO, D. RICHARDSON, Y. RIKIHISA, M. RISBUD, R. RISUENO, K. RITIS, S. RIZZA, R. RIZZUTO, H. ROBERTS, L. ROBERTS, K. ROBINSON, M. ROCCHERI, S. ROCCHI, G. RODNEY, T. RODRIGUES, V. SILVA, A. RODRIGUEZ, R. RODRIGUEZ-BARRUECO, N. RODRIGUEZ-HENCHE, H. RODRIGUEZ-ROCHA, J. ROELOFS, R. ROGERS, V. ROGOV, A. ROJO, K. ROLKA, V. ROMANELLO, L. ROMANI, A. ROMANO, P. ROMANO, D. ROMEO-GUITART, L. ROMERO, M. ROMERO, J. RONEY, C. RONGO, S. ROPERTO, M. ROSENFELDT, P. ROSENSTIEL, A. ROSENWALD, K. ROTH, L. ROTH, S. ROTH, K. ROUSCHOP, B. ROUSSEL, S. ROUX, P. ROVERE-QUERINI, A. ROY, A. ROZIERES, D. RUANO, D. RUBINSZTEIN, M. RUBTSOVA, K. RUCKDESCHEL, C. RUCKENSTUHL, E. RUDOLF, R. RUDOLF, A. RUGGIERI, A. RUPARELIA, P. RUSMINI, R. RUSSELL, G. RUSSO, M. RUSSO, R. RUSSO, O. RYABAYA, K. RYAN, K. RYU, M. SABATER-ARCIS, U. SACHDEV, M. SACHER, C. SACHSE, A. SADHU, J. SADOSHIMA, N. SAFREN, P. SAFTIG, A. SAGONA, G. SAHAY, A. SAHEBKAR, M. SAHIN, O. SAHIN, S. SAHNI, N. SAITO, S. SAITO, T. SAITO, R. SAKAI, Y. SAKAI, J. SAKAMAKI, K. SAKSELA, G. SALAZAR, A. SALAZAR-DEGRACIA, G. SALEKDEH, A. SALUJA, B. SAMPAIO-MARQUES, M. SANCHEZ, J. SANCHEZ-ALCAZAR, V. SANCHEZ-VERA, V. SANCHO-SHIMIZU, J. SANDERSON, M. SANDRI, S. SANTAGUIDA, L. SANTAMBROGIO, M. SANTANA, G. SANTONI, A. SANZ, P. SANZ, S. SARAN, M. SARDIELLO, T. SARGEANT, A. SARIN, C. SARKAR, S. SARKAR, M. SARRIAS, D. SARMAH, J. SARPARANTA, A. SATHYANARAYAN, R. SATHYANARAYANAN, K. SCAGLIONE, F. SCATOZZA, L. SCHAEFER, Z. SCHAFER, U. SCHAIBLE, A. SCHAPIRA, M. SCHARL, H. SCHATZL, C. SCHEIN, W. SCHEPER, D. SCHEURING, M. SCHIAFFINO, M. SCHIAPPACASSI, R. SCHINDL, U. SCHLATTNER, O. SCHMIDT, R. SCHMITT, S. SCHMIDT, I. SCHMITZ, E. SCHMUKLER, A. SCHNEIDER, B. SCHNEIDER, R. SCHOBER, A. SCHOIJET, M. SCHOTT, M. SCHRAMM, B. SCHRODER, K. SCHUH, C. SCHULLER, R. SCHULZE, L. SCHURMANNS, J. SCHWAMBORN, M. SCHWARTEN, F. SCIALO, S. SCIARRETTA, M. 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SKENDROS, A. SKIRYCZ, I. SLANINOVA, S. SMAILI, A. SMERTENKO, M. SMITH, S. SOENEN, E. SOHN, S. SOK, G. SOLAINI, T. SOLDATI, S. SOLEIMANPOUR, R. SOLER, A. SOLOVCHENKO, J. SOMARELLI, A. SONAWANE, F. SONG, H. SONG, J. SONG, K. SONG, Z. SONG, L. SORIA, M. SORICE, A. SOUKAS, S. SOUKUP, D. SOUSA, N. SOUSA, P. SPAGNUOLO, S. SPECTOR, M. BHARATH, D. ST CLAIR, V. STAGNI, L. STAIANO, C. STALNECKER, M. STANKOV, P. STATHOPULOS, K. STEFAN, S. STEFAN, L. STEFANIS, J. STEFFAN, A. STEINKASSERER, H. STENMARK, J. STERNECKERT, C. STEVENS, V. STOKA, S. STORCH, B. STORK, F. STRAPPAZZON, A. STROHECKER, D. STUPACK, H. SU, L. SU, A. SUAREZFONTES, C. SUBAUSTE, S. SUBBIAN, P. SUBIRADA, G. SUDHANDIRAN, C. SUE, X. SUI, C. SUMMERS, G. SUN, J. SUN, K. SUN, M. SUN, Q. SUN, Y. SUN, Z. SUN, K. SUNAHARA, E. SUNDBERG, K. SUSZTAK, P. SUTOVSKY, H. SUZUKI, G. SWEENEY, J. SYMONS, S. SZE, N. SZEWCZYK, C. TABOLACCI, F. TACKE, H. TAEGTMEYER, M. TAFANI, M. TAGAYA, H. TAI, S. TAIT, Y. TAKAHASHI, S. TAKATS, P. TALWAR, C. TAM, S. TAM, D. TAMPELLINI, A. TAMURA, C. TAN, E. TAN, Y. TAN, M. TANAKA, D. TANG, J. TANG, T. TANG, I. TANIDA, Z. TAO, M. TAOUIS, L. TATENHORST, N. TAVERNARAKIS, A. TAYLOR, G. TAYLOR, J. TAYLOR, E. TCHETINA, A. TEE, I. TEGEDER, D. TEIS, N. TEIXEIRA, F. TEIXEIRA-CLERC, K. TEKIRDAG, T. TENCOMNAO, S. TENREIRO, A. TEPIKIN, P. TESTILLANO, G. TETTAMANTI, P. THARAUX, K. THEDIECK, A. THEKKINGHAT, S. THELLUNG, J. THINWA, V. THIRUMALAIKUMAR, S. THOMAS, P. THOMES, A. THORBURN, L. THUKRAL, T. THUM, M. THUMM, L. TIAN, A. TICHY, A. TILL, V. TIMMERMAN, V. TITORENKO, S. TODI, K. TODOROVA, J. TOIVONEN, L. TOMAIPITINCA, D. TOMAR, C. TOMAS-ZAPICO, B. TONG, C. TONG, X. TONG, S. TOOZE, M. TORGERSEN, S. TORII, L. TORRES-LOPEZ, A. TORRIGLIA, C. TOWERS, R. TOWNS, S. TOYOKUNI, V. TRAJKOVIC, D. TRAMONTANO, Q. TRAN, L. TRAVASSOS, C. TRELFORD, S. TREMEL, I. TROUGAKOS, B. TSAO, M. TSCHAN, H. TSE, T. TSE, H. TSUGAWA, A. TSVETKOV, D. TUMBARELLO, Y. TUMTAS, M. TUNON, S. TURCOTTE, B. TURK, V. TURK, B. TURNER, R. 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ZHANG, W. ZHANG, X. ZHANG, Y. ZHANG, Z. ZHANG, H. ZHAO, L. ZHAO, S. ZHAO, T. ZHAO, X. ZHAO, Y. ZHAO, G. ZHENG, K. ZHENG, L. ZHENG, S. ZHENG, X. ZHENG, Y. ZHENG, Z. ZHENG, B. ZHIVOTOVSKY, Q. ZHONG, A. ZHOU, B. ZHOU, C. ZHOU, G. ZHOU, H. ZHOU, J. ZHOU, K. ZHOU, R. ZHOU, X. ZHOU, Y. ZHOU, Z. ZHOU, B. ZHU, C. ZHU, G. ZHU, H. ZHU, W. ZHU, Y. ZHU, H. ZHUANG, X. ZHUANG, K. ZIENTARA-RYTTER, C. ZIMMERMANN, E. ZIVIANI, T. ZOLADEK, W. ZONG, D. ZOROV, A. ZORZANO, W. ZOU, Z. ZOU, S. ZURYN, W. ZWERSCHKE, B. BRAND-SABERI, C. KENCHAPPA, S. OSHIMA, Y. RONG, J. SLUIMER, and C. STALLINGS
Subjects: flux, macroautophagy, phagophore, stress, vacuole, Autophagosome, LC3, lysosome, neurodegeneration, cancer
Abstract: In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Published: 2021

46. COVID Response: The Money Market Mutual Fund Facility

Author: Kenechukwu Anadu, Marco Cipriani, Ryan Craver, and Gabriele La Spada
Published: 2021

47. Deep Learning Techniques and COVID-19 Drug Discovery: Fundamentals, State-of-the-Art and Future Directions

Author: Hamed Hashemi-Dezaki, Saeedeh Lotfi, Luigi La Spada, Mojgan Dehghani, Morteza Jamshidi, Asal Sabet, Mohammad Mahdi Honari, Pedram Lalbakhsh, Mirhamed Mirmozafari, Saeed Roshani, Jakub Talla, Zahra Malek, Mohammad Jamshidi, Alireza Jamshidi, Ali Lalbakhsh, Sobhan Roshani, Zdeněk Peroutka, Farimah Hadjilooei, Václav Matoušek, and Sahar Ahmadi
Subjects: Hopfield network, Deep belief network, Restricted Boltzmann machine, Drug development, Artificial neural network, Process (engineering), business.industry, Computer science, Deep learning, State (computer science), Artificial intelligence, business, Data science
Abstract: The world is in a frustrating situation, which is exacerbating due to the time-consuming process of the COVID-19 vaccine design and production. This chapter provides a comprehensive investigation of fundamentals, state-of-the-art and some perspectives to speed up the process of the design, optimization and production of the medicine for COVID-19 based on Deep Learning (DL) methods. The proposed platforms are able to be used as predictors to forecast antigens during the infection disregarding their abundance and immunogenicity with no requirement of growing the pathogen in vitro. First, we briefly survey the latest achievements and fundamentals of some DL methodologies, including Deep Boltzmann Machines (DBM), Restricted Boltzmann Machine (RBM), Deep Belief Network (DBN), Hopfield network and Long Short-Term Memory(LSTM). These techniques help us to reach an integrated approach for drug development by non-conventional antigens. We then propose several DL-based platforms to utilize for future applications regarding the latest publications and medical reports. Considering the evolving date on COVID-19 and its ever-changing nature, we believe this survey can give readers some useful ideas and directions to understand the application of Artificial Intelligence (AI) to accelerate the vaccine design not only for COVID-19 but also for many different diseases or viruses.
Published: 2021

48. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Author: Klionsky D, Abdel-Aziz A, Abdelfatah S, Abdellatif M, Abdoli A, Abel S, Abeliovich H, Abildgaard M, Abudu Y, Acevedo-Arozena A, Adamopoulos I, Adeli K, Adolph T, Adornetto A, Aflaki E, Agam G, Agarwal A, Aggarwal B, Agnello M, Agostinis P, Agrewala J, Agrotis A, Aguilar P, Ahmad S, Ahmed Z, Ahumada-Castro U, Aits S, Aizawa S, Akkoc Y, Akoumianaki T, Akpinar H, Al-Abd A, Al-Akra L, Al-Gharaibeh A, Alaoui-Jamali M, Alberti S, Alcocer-Gomez E, Alessandri C, Ali M, Al-Bari M, Aliwaini S, Alizadeh J, Almacellas E, Almasan A, Alonso A, Alonso G, Altan-Bonnet N, Altieri D, Alves S, da Costa C, Alzaharna M, Amadio M, Amantini C, Amaral C, Ambrosio S, Amer A, Ammanathan V, An Z, Andersen S, Andrabi S, Andrade-Silva M, Andres A, Angelini S, Ann D, Anozie U, Ansari M, Antas P, Antebi A, Anton Z, Anwar T, Apetoh L, Apostolova N, Araki T, Araki Y, Arasaki K, Araujo W, Araya J, Arden C, Arevalo M, Arguelles S, Arias E, Arikkath J, Arimoto H, Ariosa A, Armstrong-James D, Arnaune-Pelloquin L, 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Subjects: flux, macroautophagy, phagophore, stress, vacuole, Autophagosome, LC3, lysosome, neurodegeneration, cancer
Abstract: In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Published: 2021

49. The Market Events of Mid-September 2019

Author: Antoine Martin, Anna Kovner, Gabriele La Spada, Marco Cipriani, Adam Copeland, and Gara Afonso
Subjects: Money market, History, Polymers and Plastics, media_common.quotation_subject, Monetary policy, Financial system, Industrial and Manufacturing Engineering, Fixed income, Open market operation, Federal funds, Cash, Intermediation, Interbank lending market, Business, Business and International Management, media_common
Abstract: This paper studies the mid-September 2019 stress in U.S. money markets: On September 16 and 17, unsecured and secured funding rates spiked up and, on September 17, the effective federal funds rate broke the ceiling of the Federal Open Market Committee (FOMC) target range. We highlight two factors that may have contributed to these events. First, reserves may have become scarce for at least some depository institutions, in the sense that these institutions’ reserve holdings may have been close to, or lower than, their desired level. Moreover, frictions in the interbank market may have prevented the efficient allocation of reserves across institutions, so that although aggregate reserves may have been higher than the sum of reserves demanded by each institution, they were still scarce given the market’s inability to allocate reserves efficiently. Second, we provide evidence that some large domestic dealers likely experienced an increase in intermediation costs, which led them to charge higher spreads to ultimate cash borrowers. This increase was due to a temporary reduction in lending from money market mutual funds, including through the Fixed Income Clearing Corporation’s (FICC’s) sponsored repo program.
Published: 2021

50. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

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Yoshimori T, Yousefi B, Yu B, Yu H, Yu J, Yu L, Yu ML, Yu SW, Yu VC, Yu WH, Yu Z, Yuan J, Yuan LQ, Yuan S, Yuan SF, Yuan Y, Yuan Z, Yue J, Yue Z, Yun J, Yung RL, Zacks DN, Zaffagnini G, Zambelli VO, Zanella I, Zang QS, Zanivan S, Zappavigna S, Zaragoza P, Zarbalis KS, Zarebkohan A, Zarrouk A, Zeitlin SO, Zeng J, Zeng JD, Žerovnik E, Zhan L, Zhang B, Zhang DD, Zhang H, Zhang HL, Zhang J, Zhang JP, Zhang KYB, Zhang LW, Zhang L, Zhang M, Zhang P, Zhang S, Zhang W, Zhang X, Zhang XW, Zhang XD, Zhang Y, Zhang YD, Zhang YY, Zhang Z, Zhao H, Zhao L, Zhao S, Zhao T, Zhao XF, Zhao Y, Zheng G, Zheng K, Zheng L, Zheng S, Zheng XL, Zheng Y, Zheng ZG, Zhivotovsky B, Zhong Q, Zhou A, Zhou B, Zhou C, Zhou G, Zhou H, Zhou J, Zhou K, Zhou R, Zhou XJ, Zhou Y, Zhou ZY, Zhou Z, Zhu B, Zhu C, Zhu GQ, Zhu H, Zhu WG, Zhu Y, Zhuang H, Zhuang X, Zientara-Rytter K, Zimmermann CM, Ziviani E, Zoladek T, Zong WX, Zorov DB, Zorzano A, Zou W, Zou Z, Zuryn S, Zwerschke W, Brand-Saberi B, Dong XC, Kenchappa CS, Lin Y, Oshima S, Rong Y, Sluimer JC, Stallings CL, and Tong CK
Subjects: flux, macroautophagy, phagophore, stress, vacuole, Autophagosome, LC3, lysosome, neurodegeneration, cancer
Abstract: In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Published: 2021

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