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2. Regulation of Zbp1 by miR-99b-5p in microglia controls the development of schizophrenia-like symptoms in mice

Author

Kaurani, Lalit, Islam, Md Rezaul, Heilbronner, Urs, Krüger, Dennis M, Zhou, Jiayin, Methi, Aditi, Strauss, Judith, Pradhan, Ranjit, Schröder, Sophie, Burkhardt, Susanne, Schuetz, Anna-Lena, Pena, Tonatiuh, Erlebach, Lena, Bühler, Anika, Budde, Monika, Senner, Fanny, Kohshour, Mojtaba Oraki, Schulte, Eva C, Schmauß, Max, Reininghaus, Eva Z, Juckel, Georg, Kronenberg-Versteeg, Deborah, Delalle, Ivana, Odoardi, Francesca, Flügel, Alexander, Schulze, Thomas G, Falkai, Peter, Sananbenesi, Farahnaz, and Fischer, Andre

Published
2024
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3. Cortical-sparing chronic traumatic encephalopathy (CSCTE): a distinct subtype of CTE

Author

Alexander, Abigail, Alvarez, Victor E., Huber, Bertrand R., Alosco, Michael L., Mez, Jesse, Tripodis, Yorghos, Nicks, Raymond, Katz, Douglas I., Dwyer, Brigid, Daneshvar, Daniel H., Martin, Brett, Palmisano, Joseph, Goldstein, Lee E., Crary, John F., Nowinski, Christopher, Cantu, Robert C., Kowall, Neil W., Stern, Robert A., Delalle, Ivana, McKee, Ann C., and Stein, Thor D.

Published
2024
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5. Methionine Sulfoxide Reductase-B3 Risk Allele Implicated in Alzheimer’s Disease Associates with Increased Odds for Brain Infarcts

Author

Conner, Sarah C, Benayoun, Laurent, Himali, Jayandra J, Adams, Stephanie L, Yang, Qiong, DeCarli, Charles, Blusztajn, Jan K, Beiser, Alexa, Seshadri, Sudha, and Delalle, Ivana

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Genetics, Brain Disorders, Acquired Cognitive Impairment, Alzheimer's Disease, Neurodegenerative, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Dementia, Aging, Aetiology, 2.1 Biological and endogenous factors, Neurological, Aged, Alleles, Brain Infarction, Female, Genetic Predisposition to Disease, Hippocampus, Humans, Incidence, Magnetic Resonance Imaging, Male, Methionine Sulfoxide Reductases, Middle Aged, Polymorphism, Single Nucleotide, Framingham Heart Study, hippocampus, MSRB3, vascular pathology, Cognitive Sciences, Neurology & Neurosurgery, Clinical sciences, Biological psychology
Abstract

Genome-wide association studies identified a single nucleotide polymorphism (SNP) in the MSRB3 gene encoding Methionine Sulfoxide Reductase-B3 (MsrB3) to be associated with the risk for low hippocampal volume and late onset Alzheimer's disease (AD). Subsequently, we identified AD-associated abnormal patterns of neuronal and vascular MsrB3 expression in postmortem hippocampi. The present study investigated the relationship between the MSRB3 SNP rs61921502, G (minor/risk allele) and MRI measures of brain injury including total brain volume, hippocampal volume, and white matter hyperintensities using linear regression models; the presence of brain infarcts using logistic regression models; and the incidence of stroke, dementia, and AD using Cox proportional hazards models in 2,038 Framingham Heart Study Offspring participants with MRI administered close to examination cycle 7 (1998-2001). Participants with neurological conditions that impede evaluation of vascular pathology by MRI, i.e., brain tumors, multiple sclerosis, and major head trauma, were excluded from the study. When adjusted for age and age squared at MRI exam, sex, and presence of Apolipoproteinɛ4 allele (APOE4), individuals with MSRB3 rs61921502 minor allele had increased odds for brain infarcts on MRI compared to those with no minor allele. However, in stratified analyses, MSRB3 rs61921502 minor allele was significantly associated with increased odds for MRI brain infarcts only in the absence of APOE4.

Published
2019

7. HDAC1 links early life stress to schizophrenia-like phenotypes

Author

Bahari-Javan, Sanaz, Varbanov, Hristo, Halder, Rashi, Benito, Eva, Kaurani, Lalit, Burkhardt, Susanne, Anderson-Schmidt, Heike, Anghelescu, Ion, Budde, Monika, Stilling, Roman M., Costa, Joan, Medina, Juan, Dietrich, Detlef E., Figge, Christian, Folkerts, Here, Gade, Katrin, Heilbronner, Urs, Koller, Manfred, Konrad, Carsten, Nussbeck, Sara Y., Scherk, Harald, Spitzer, Carsten, Stierl, Sebastian, Stöckel, Judith, Thiel, Andreas, von Hagen, Martin, Zimmermann, Jörg, Zitzelsberger, Antje, Schulz, Sybille, Schmitt, Andrea, Delalle, Ivana, Falkai, Peter, Schulze, Thomas G., Dityatev, Alexander, Sananbenesi, Farahnaz, and Fischer, André

Published
2017

8. A novel miR-99b-5p-Zbp1 pathway in microglia contributes to the pathogenesis of schizophrenia

Author

Kaurani, Lalit, primary, Islam, Md Rezaul, additional, Heilbronner, Urs, additional, Krüger, Dennis M., additional, Zhou, Jiayin, additional, Methi, Aditi, additional, Strauss, Judith, additional, Pradhan, Ranjit, additional, Burkhardt, Susanne, additional, Pena, Tonatiuh, additional, Erlebach, Lena, additional, Bühler, Anika, additional, Budde, Monika, additional, Senner, Fanny, additional, Kohshour, Mojtaba Oraki, additional, Schulte, Eva C., additional, Schmauß, Max, additional, Reininghaus, Eva Z., additional, Juckel, Georg, additional, Kronenberg-Versteeg, Deborah, additional, Delalle, Ivana, additional, Odoardi, Francesca, additional, Flügel, Alexander, additional, Schulze, Thomas G., additional, Falkai, Peter, additional, Sananbenesi, Farahnaz, additional, and Fischer, Andre, additional

Published
2023
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9. A combined miRNA–piRNA signature to detect Alzheimer’s disease

Author

Jain, Gaurav, Stuendl, Anne, Rao, Pooja, Berulava, Tea, Pena Centeno, Tonatiuh, Kaurani, Lalit, Burkhardt, Susanne, Delalle, Ivana, Kornhuber, Johannes, Hüll, Michael, Maier, Wolfgang, Peters, Oliver, Esselmann, Hermann, Schulte, Claudia, Deuschle, Christian, Synofzik, Mathis, Wiltfang, Jens, Mollenhauer, Brit, Maetzler, Walter, Schneider, Anja, and Fischer, Andre

Published
2019
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11. Conserved reduction of m 6 A RNA modifications during aging and neurodegeneration is linked to changes in synaptic transcripts

Author

Castro-Hernández, Ricardo, primary, Berulava, Tea, additional, Metelova, Maria, additional, Epple, Robert, additional, Peña Centeno, Tonatiuh, additional, Richter, Julia, additional, Kaurani, Lalit, additional, Pradhan, Ranjit, additional, Sakib, M. Sadman, additional, Burkhardt, Susanne, additional, Ninov, Momchil, additional, Bohnsack, Katherine E., additional, Bohnsack, Markus T., additional, Delalle, Ivana, additional, and Fischer, Andre, additional

Published
2023
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16. Conserved reduction of m6A marks during aging and neurodegeneration is linked to altered translation of synaptic transcripts

Author

Castro-Hernández, Ricardo, primary, Berulava, Tea, additional, Metelova, Maria, additional, Epple, Robert, additional, Centeno, Tonatiuh Peña, additional, Sakib, M Sadman, additional, Burkhart, Susanne, additional, Ninov, Momchil, additional, Bohnsack, Katherine E., additional, Bohnsack, Markus T., additional, Delalle, Ivana, additional, and Fischer, Andre, additional

Published
2022
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18. Conserved reduction of m6 A RNA modifications during aging and neurodegeneration is linked to changes in synaptic transcripts.

Author

Castro-Hernández, Ricardo, Berulava, Tea, Metelova, Maria, Epple, Robert, Centeno, Tonatiuh Peña, Richter, Julia, Kaurani, Lalit, Pradhan, Ranjit, Sakib, M. Sadman, Burkhardt, Susanne, Ninov, Momchil, Bohnsack, Katherine E., Bohnsack, Markus T., Delalle, Ivana, and Fischer, Andre

Subjects
RNA modification & restriction, ALZHEIMER'S patients, RNA methylation, CINGULATE cortex, ALZHEIMER'S disease, DENTATE gyrus
Abstract

N6 -methyladenosine (m6 A) regulates mRNA metabolism. While it has been implicated in the development of the mammalian brain and in cognition, the role of m6 A in synaptic plasticity, especially during cognitive decline, is not fully understood. In this study, we employed methylated RNA immunoprecipitation sequencing to obtain the m6 A epitranscriptome of the hippocampal subregions CA1, CA3, and the dentate gyrus and the anterior cingulate cortex (ACC) in young and aged mice. We observed a decrease in m6 A levels in aged animals. Comparative analysis of cingulate cortex (CC) brain tissue from cognitively intact human subjects and Alzheimer’s disease (AD) patients showed decreased m6 A RNA methylation in AD patients. m6 A changes common to brains of aged mice and AD patients were found in transcripts linked to synaptic function including calcium/calmodulin-dependent protein kinase 2 (CAMKII) and AMPA-selective glutamate receptor 1 (Glua1). We used proximity ligation assays to show that reduced m6 A levels result in decreased synaptic protein synthesis as exemplified by CAMKII and GLUA1. Moreover, reduced m6 A levels impaired synaptic function. Our results suggest that m6 A RNA methylation controls synaptic protein synthesis and may play a role in cognitive decline associated with aging and AD. [ABSTRACT FROM AUTHOR]

Published
2023
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21. MICRORNAS AS CANDIDATES FOR BIPOLAR DISORDER BIOMARKERS

Author

Delalle, Ivana

Subjects
epigenetic regulation, psychoses, exosomes, human brain
Abstract

Bipolar disorder (BD) is a common, recurring psychiatric illness with unknown pathogenesis. Much like other psychiatric diseases, BD suffers from the chronic lack of reliable biomarkers and innovative pharmacological interventions. Better characterization of clinical profiles, experimental medicine, genomic data mining, and the utilization of experimental models, including stem cell and genetically modified mice, are suggested ways forward. Environment, including early childhood experiences, has been documented to modulate the risk for the development of psychiatric disorders via epigenetic mechanisms. Key epigenetic regulators, microRNAs (miRNAs, miRs), govern normal neuronal functioning and show altered expression in diverse brain pathologies. We observed significant alterations of exosomal miR-29c levels in prefrontal cortex (Brodmann area 9, BA9) of BD patients. We also demonstrated that exosomes extracted from the anterior cingulate cortex (BA24), a crucial area for modulating emotional expression and affect, have increased levels of miR-149 in BD patients compared to controls. Because miR-149 has been shown to inhibit glial proliferation, we hypothesized that increased miR-149 expression in BA24-derived exosomes may be consistent with the previously reported reduced glial cell numbers in BA24 of patients diagnosed with familial BD. qPCR analysis of laser-microdissected neuronal and glial cells from BA24 cortical samples of BD patients verified that the glial, but not neuronal, population exhibits significantly increased miR-149 expression. These findings support neuron-glia interaction as a possible target mechanism in BD, implicated by others in neuroimaging, postmortem, and in vivo studies of the pathological changes mediated by glial cells.

Published
2021

22. An epigenetic blockade of cognitive functions in the neurodegenerating brain

Author

Graff, Johannes, Rei, Damien, Guan, Ji-Song, Wang, Wen-Yuan, Seo, Jinsoo, Hennig, Krista M., Nieland, Thomas J.F., Fass, Daniel M., Kao, Patricia F., Kahn, Martin, Su, Susan C., Samiei, Alireza, Joseph, Nadine, Haggarty, Stephen J., Delalle, Ivana, and Tsai, Li-Huei

Subjects
Nervous system -- Degeneration, Epigenetic inheritance -- Health aspects, Cognition disorders -- Genetic aspects -- Causes of, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Cognitive decline is a debilitating feature of most neurodegenerative diseases of the central nervous system, including Alzheimer's disease (1). The causes leading to such impairment are only poorly understood and effective treatments are slow to emerge (2). Here we show that cognitive capacities in the neurodegenerating brain are constrained by an epigenetic blockade of gene transcription that is potentially reversible. This blockade is mediated by histone deacetylase 2, which is increased by Alzheimer's-disease-related neurotoxic insults in vitro, in two mouse models of neurodegeneration and in patients with Alzheimer's disease. Histone deacetylase 2 associates with and reduces the histone acetylation of genes important for learning and memory, which show a concomitant decrease in expression. Importantly, reversing the build-up of histone deacetylase 2 by short-hairpin-RNA-mediated knockdown unlocks the repression of these genes, reinstates structural and synaptic plasticity, and abolishes neurodegeneration-associated memory impairments. These findings advocate for the development of selective inhibitors of histone deacetylase 2 and suggest that cognitive capacities following neurodegeneration are not entirely lost, but merely impaired by this epigenetic blockade., Long-lasting forms of memories require stable gene expression changes (3), which are in part orchestrated by chromatin-templated epigenetic processes (4). Of the epigenetic modifications identified so far in the nervous [...]

Published
2012
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23. microRNA‐34c is a novel target to treat dementias

Author

Zovoilis, Athanasios, Agbemenyah, Hope Y, Agis‐Balboa, Roberto C, Stilling, Roman M, Edbauer, Dieter, Rao, Pooja, Farinelli, Laurent, Delalle, Ivana, Schmitt, Andrea, Falkai, Peter, Bahari‐Javan, Sanaz, Burkhardt, Susanne, Sananbenesi, Farahnaz, and Fischer, Andre

Published
2011
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29. Mutations in the drosophila orthologs of the F-actin capping protein [alpha]- and [beta]-subunits cause actin accumulation and subsequent retinal degeneration

Author

Delalle, Ivana, Pfleger, Cathie M., Buff, Eugene, Lueras, Paula, and Hariharan, Iswar K.

Subjects
Proteins -- Physiological aspects, Drosophila -- Physiological aspects, Biological sciences
Abstract

The progression of several human neurodegenerative diseases is characterized by the appearance of intracellular inclusions or cytoskeletal abnormalities. An important question is whether these abnormalities actually contribute to the degenerative process or whether they are merely manifestations of cells that are already destined for degeneration. We have conducted a large screen in Drosophila for mutations that alter the growth or differentiation of cells during eye development. We have used mitotic recombination to generate patches of homozygous mutant cells. In our entire screen, mutations in only two different loci, burned (bnd) and scorched (scrd), resulted in eyes in which the mutant patches appeared black and the mutant tissue appeared to have undergone degeneration. In larval imaginal discs, growth and cell fate specification occur normally in mutant cells, but there is an accumulation of F-actin. Mutant cells degenerate much later during the pupal phase of development, burned mutations are allelic to mutations in the previously described cpb locus that encodes the [beta]-subunit of the F-actin capping protein, while scorched mutations disrupt the gene encoding its [alpha]-subunit (cpa). The [alpha]/[beta]-heterodimer caps the barbed ends of an actin filament and restricts its growth. In its absence, cells progressively accumulate actin filaments and eventually die. A possible role for their human orthologs in neurodegenerative disease merits further investigation.

Published
2005

30. A 52-year-old woman with recurrent unsteadiness, slurred speech, and fatigue

Author

Alderson, Lloyd M. and Delalle, Ivana

Subjects
Brain cancer -- Case studies, Lymphomas -- Case studies
Abstract

A 52-year-old woman with extreme fatigue and a movement disorder called ataxia was diagnosed with a brain cancer called lymphoma. Despite chemotherapy, she died eight months later.

Published
2002

35. p35 is a neural-specific regulatory subunit of cyclin-dependent kinase 5

Author

Tsai, Li-Huei, Delalle, Ivana, Caviness, Verne S., Jr., Chae, Teresa, and Harlow, Ed.

Subjects
Protein kinases -- Observations, Biological control systems -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The cloning and characterization of p35, a neural specific regulatory subunit of cyclin-dependent kinase 5 (Cdk5), reveals the presence of neuronal cell-specific type of expression. The p35 is also associated with the activities of the Cdk5 kinase and is different from mammalian cyclins in function. The p35 is a new type of regulatory subunit with a structural homology for regulation of cell cycle progression.

Published
1994

41. Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia

Author

Agís‐Balboa, Roberto Carlos, primary, Pinheiro, Paulo S, additional, Rebola, Nelson, additional, Kerimoglu, Cemil, additional, Benito, Eva, additional, Gertig, Michael, additional, Bahari‐Javan, Sanaz, additional, Jain, Gaurav, additional, Burkhardt, Susanne, additional, Delalle, Ivana, additional, Jatzko, Alexander, additional, Dettenhofer, Markus, additional, Zunszain, Patricia A, additional, Schmitt, Andrea, additional, Falkai, Peter, additional, Pape, Julius C, additional, Binder, Elisabeth B, additional, Mulle, Christophe, additional, Fischer, Andre, additional, and Sananbenesi, Farahnaz, additional

Published
2017
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42. GENE-09. PRECISION MEDICINE ANALYSIS OF 203 PEDIATRIC BRAIN TUMORS REVEALS CLINICALLY RELEVANT GENOMIC ALTERATIONS

Author

Bandopadhayay, Pratiti, primary, Ramkissoon, Shakti, additional, Hwang, Jaeho, additional, Ramkissoon, Lori, additional, Greenwald, Noah, additional, Schumacher, Steven, additional, O’Rourke, Ryan, additional, Pinches, Nathan, additional, Ho, Patricia, additional, Malkin, Hayley, additional, Sinai, Claire, additional, Filbin, Mariella, additional, Plant, Ashley, additional, Bi, Wenya, additional, Chang, Michael, additional, Yang, Edward, additional, Wright, Karen, additional, Manley, Peter, additional, Ducar, Matthew, additional, Alexandrescu, Sanda, additional, Lidov, Hart, additional, Delalle, Ivana, additional, Goumnerova, Liliana, additional, Church, Alanna, additional, Janeway, Katherine, additional, Harris, Marian, additional, MacConaill, Laura, additional, Folkerth, Rebecca, additional, Lindeman, Neal, additional, Stiles, Charles, additional, Kieran, Mark, additional, Ligon, Azra, additional, Santagata, Sandro, additional, Dubuc, Adrian, additional, Chi, Susan, additional, Beroukhim, Rameen, additional, and Ligon, Keith, additional

Published
2017
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43. Monoaminergic neuropathology in Alzheimer’s disease

Author

Šimić, Goran, primary, Babić Leko, Mirjana, additional, Wray, Selina, additional, Harrington, Charles R., additional, Delalle, Ivana, additional, Jovanov-Milošević, Nataša, additional, Bažadona, Danira, additional, Buée, Luc, additional, de Silva, Rohan, additional, Di Giovanni, Giuseppe, additional, Wischik, Claude M., additional, and Hof, Patrick R., additional

Published
2017
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44. miR‐149 and miR‐29c as candidates for bipolar disorder biomarkers

Author

Choi, Jason L., primary, Kao, Patricia F., additional, Itriago, Elena, additional, Zhan, Yougen, additional, Kozubek, James A., additional, Hoss, Andrew G., additional, Banigan, Meredith G., additional, Vanderburg, Charles R., additional, Rezvani, Amir H., additional, Latourelle, Jeanne C., additional, Cabral, Howard, additional, and Delalle, Ivana, additional

Published
2017
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45. Clinical targeted exome-based sequencing in combination with genome-wide copy number profiling: precision medicine analysis of 203 pediatric brain tumors

Author

Ramkissoon, Shakti H., primary, Bandopadhayay, Pratiti, additional, Hwang, Jaeho, additional, Ramkissoon, Lori A., additional, Greenwald, Noah F., additional, Schumacher, Steven E., additional, O’Rourke, Ryan, additional, Pinches, Nathan, additional, Ho, Patricia, additional, Malkin, Hayley, additional, Sinai, Claire, additional, Filbin, Mariella, additional, Plant, Ashley, additional, Bi, Wenya Linda, additional, Chang, Michael S., additional, Yang, Edward, additional, Wright, Karen D., additional, Manley, Peter E., additional, Ducar, Matthew, additional, Alexandrescu, Sanda, additional, Lidov, Hart, additional, Delalle, Ivana, additional, Goumnerova, Liliana C., additional, Church, Alanna J., additional, Janeway, Katherine A., additional, Harris, Marian H., additional, MacConaill, Laura E., additional, Folkerth, Rebecca D., additional, Lindeman, Neal I., additional, Stiles, Charles D., additional, Kieran, Mark W., additional, Ligon, Azra H., additional, Santagata, Sandro, additional, Dubuc, Adrian M., additional, Chi, Susan N., additional, Beroukhim, Rameen, additional, and Ligon, Keith L., additional

Published
2017
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47. Down Syndrome Developmental Brain Transcriptome Reveals Defective Oligodendrocyte Differentiation and Myelination

Author

Olmos-Serrano, Jose Luis, primary, Kang, Hyo Jung, additional, Tyler, William A., additional, Silbereis, John C., additional, Cheng, Feng, additional, Zhu, Ying, additional, Pletikos, Mihovil, additional, Jankovic-Rapan, Lucija, additional, Cramer, Nathan P., additional, Galdzicki, Zygmunt, additional, Goodliffe, Joseph, additional, Peters, Alan, additional, Sethares, Claire, additional, Delalle, Ivana, additional, Golden, Jeffrey A., additional, Haydar, Tarik F., additional, and Sestan, Nenad, additional

Published
2016
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48. Tau Protein Hyperphosphorylation and Aggregation in Alzheimer’s Disease and Other Tauopathies, and Possible Neuroprotective Strategies

Author

Šimić, Goran, primary, Babić Leko, Mirjana, additional, Wray, Selina, additional, Harrington, Charles, additional, Delalle, Ivana, additional, Jovanov-Milošević, Nataša, additional, Bažadona, Danira, additional, Buée, Luc, additional, de Silva, Rohan, additional, Di Giovanni, Giuseppe, additional, Wischik, Claude, additional, and Hof, Patrick, additional

Published
2016
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49. An epigenetic blockade of cognitive functions in the neurodegenerating brain

Author

Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Picower Institute for Learning and Memory, Graff, Johannes, Rei, Damien, Guan, Ji-Song, Wang, Wen-Yuan, Seo, Jinsoo, Su, Susan C., Joseph, Nadine, Tsai, Li-Huei, Kahn, Martin, Samiei, Alireza, Hennig, Krista M., Nieland, Thomas J., Fass, Daniel M., Kao, Patricia F., Haggarty, Stephen J., Delalle, Ivana, Harvard University--MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Picower Institute for Learning and Memory, Graff, Johannes, Rei, Damien, Guan, Ji-Song, Wang, Wen-Yuan, Seo, Jinsoo, Su, Susan C., Joseph, Nadine, Tsai, Li-Huei, Kahn, Martin, Samiei, Alireza, Hennig, Krista M., Nieland, Thomas J., Fass, Daniel M., Kao, Patricia F., Haggarty, Stephen J., and Delalle, Ivana

Abstract

Cognitive decline is a debilitating feature of most neurodegenerative diseases of the central nervous system, including Alzheimer’s disease [superscript 1]. The causes leading to such impairment are only poorly understood and effective treatments are slow to emerge [superscript 2]. Here we show that cognitive capacities in the neurodegenerating brain are constrained by an epigenetic blockade of gene transcription that is potentially reversible. This blockade is mediated by histone deacetylase 2, which is increased by Alzheimer’s-disease-related neurotoxic insults in vitro, in two mouse models of neurodegeneration and in patients with Alzheimer’s disease. Histone deacetylase 2 associates with and reduces the histone acetylation of genes important for learning and memory, which show a concomitant decrease in expression. Importantly, reversing the build-up of histone deacetylase 2 by short-hairpin-RNA-mediated knockdown unlocks the repression of these genes, reinstates structural and synaptic plasticity, and abolishes neurodegeneration-associated memory impairments. These findings advocate for the development of selective inhibitors of histone deacetylase 2 and suggest that cognitive capacities following neurodegeneration are not entirely lost, but merely impaired by this epigenetic blockade., Stanley Medical Research Institute, National Institute of Neurological Disorders and Stroke (U.S.) (RO1NS078839), Swiss National Science Foundation, Bard Richmond (Fellowship), Simons Foundation, Theodor und Ida Herzog-Egli Foundation

Published
2015

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