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Consumer research has focused on market-mediated efforts to memorialize the past, but this overshadows the issues that arise when consumers, as nonprofessionals, make the past consumable. Consumer-driven memorialization is defined as consumer engagement with traces of the past in memoryscapes of low market-mediation that creates a complex interplay of remembering and forgetting. Based on an ethnographic study of urban exploration, we theorize that consumer-driven memorialization comprises two practices of tracing and trace-making. Tracing involves consumer attempts to recover traces of the past, while trace-making involves consumer attempts to create traces for the future. Consumers enact multiple roles during consumer-driven memorialization: explorers experience the past, archaeologists materialize the past, artists aestheticize the past, and historians narrate the past. The theorization of consumer-driven memorialization offers three contributions. First, the dimensions of consumer-driven memorialization broaden understanding of what constitutes a consumable past in contexts of low market-mediation. Second, we explain how the ideological and material challenges that emerge in consumer-driven memorialization generate a complex interplay between remembering and forgetting. Third, we shed light on how consumer-driven memorialization is inscribed in space. [ABSTRACT FROM AUTHOR]

This review's main focus is highlighting and recognizing the significant scientific advances of smart expandable lost circulation material, i.e., shape memory polymers (SMPs) composites as loss circulation material (LCM) for drilling applications as innovative and futuristic materials. This review highlights and explains ways of producing new smart materials for LCM, which can be programmed by its SMP cycle. It briefly describes loss circulation further on loss circulation material and its classification. Only very few SMPs used as LCM, like shape memory polyurethane, thermoset shape memory polymer, shape memory epoxy, etc., either used as Grout, mixed with xanthan gum, or medium-size particles combined with base fluid, while the next section focuses on shape memory polymer as loss circulation material with the shape memory effect and programming over treating wide fractures. The last section consists of conclusion, prospects, and recommendations. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and behavioral impairments. Despite extensive research efforts, effective treatment options for AD remain limited. Recently, gene therapy has emerged as a promising avenue for targeted intervention in the pathogenesis of AD. This review will provide an overview of clinical and preclinical studies where gene therapy techniques have been utilized in the context of AD, highlighting their potential as novel therapeutic strategies. While challenges remain, ongoing research and technological advancement continue to enhance the potential of gene therapy as a targeted and personalized therapeutic approach for AD. [ABSTRACT FROM AUTHOR]

[Display omitted] • EEPF inhibits Aβ aggregation and displays strong antioxidant activity. • EEPF improves memory impairment via targeting neuronal death and inflammation. • Neuroprotective action of EEPF is modulated through CaMK2/FER signaling pathway. • Anti-inflammatory effect of EEPF is regulated through Smad3/cyclin D3 pathway. Alzheimer's disease (AD) is the most common cause of dementia and is caused by various factors including amyloid-beta (Aβ) aggregation. We investigated the pharmacological effects of the ethanol extract of Potentilla fragarioides var. major (Rosaceae) (EEPF) on AD-related pathogenesis, which remain elusive. We observed the effects of EEPF on Aβ disaggregation and free-radical scavenging activities for 2,2′-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) using in vitro assays, evaluated the effects of EEPF on memory loss in two animal models, and examined the molecular regulatory mechanisms of EEPF using an antibody-protein microarray in EEPF-treated neuronal cell lines. EEPF inhibited Aβ aggregation in a concentration-dependent manner and enhanced free-radical scavenging activities for ABTS and DPPH. EEPF significantly inhibited memory impairment in the passive avoidance task, Y-maze test, and Morris water maze test in scopolamine-induced short-term memory loss mice and Aβ-injected AD-like mice. Nissl staining and immunohistochemistry for NeuN and Iba-1 confirmed the neuroprotective and anti-inflammatory effects of EEPF in both animal models. In H 2 O 2 -treated HT22 hippocampal cells, EEPF significantly prevented cell damage, enhanced CaMK2, and reduced ferric reductase. In lipopolysaccharide (LPS)-stimulated BV-2 microglia, EEPF significantly inhibited LPS-induced production of inflammatory factors, such as nitric oxide, prostaglandin E2, tumor necrosis factor-α, and interleukin-6, and decreased the phosphorylation of Smad3 and cyclin D3. High-performance liquid chromatography confirmed that EEPF has five major components: neochlorogenic acid, chlorogenic acid, polydatin, isochlorogenic acid A, and buddleoside, with amounts ranging across 1.91–9.41 mg/g. EEPF may be a promising drug for treatment of AD and AD-related brain disorders. [ABSTRACT FROM AUTHOR]

AbstractGrievers recall memories from both the life of the deceased and the dying days, but differences in recall across these memory types are not well-characterized. In this study, 100 bereaved German adults described up to ten important memories of a deceased close other (M = 7.86). Memories from the dying days were classified into: final memories, health transition events, last time events, and temporal markers. Among those who provided at least one dying days memory (73%), these memories were reported to be recalled privately and shared socially more often than memories from the deceased’s life. Memories from the dying days were rated as less emotionally positive than those from the life, and contextual factors from the loss shaped memory recall frequency and emotional valence. Results underscore the need for appropriate end-of-life care to lay a foundation for adaptive remembering and suggest the relevance of dying days memories in therapeutic settings. [ABSTRACT FROM AUTHOR]

Histone H3.3 is frequently mutated in tumors, with the lysine 36 to methionine mutation (K36M) being a hallmark of chondroblastomas. While it is known that H3.3K36M changes the epigenetic landscape, its effects on gene expression dynamics remain unclear. Here, we use a synthetic reporter to measure the effects of H3.3K36M on silencing and epigenetic memory after recruitment of the ZNF10 Krüppel-associated box (KRAB) domain, part of the largest class of human repressors and associated with H3K9me3 deposition. We find that H3.3K36M, which decreases H3K36 methylation and increases histone acetylation, leads to a decrease in epigenetic memory and promoter methylation weeks after KRAB release. We propose a model for establishment and maintenance of epigenetic memory, where the H3K36 methylation pathway is necessary to maintain histone deacetylation and convert H3K9me3 domains into DNA methylation for stable epigenetic memory. Our quantitative model can inform oncogenic mechanisms and guide development of epigenetic editing tools. [Display omitted] • H3.3K36M expression leads to reduced epigenetic memory after KRAB silencing • Epigenetic memory loss by H3.3K36M cannot be explained by reduced H3K9me3 • Inhibition of H3K36 methylases NSD1 or SETD2 phenocopies memory loss by H3.3K36M • Loss of epigenetic memory by H3.3K36M is associated with reduced CpG methylation The H3.3K36M oncohistone mutation is a driver of chondroblastomas. Sinha et al. provide evidence that expression of H3.3K36M leads to a loss of epigenetic memory in human cell models through inhibition of H3K36 methylases and concordant loss of CpG methylation. [ABSTRACT FROM AUTHOR]

The article "Memory and Amnesia" in Frontiers in Education discusses a lesson plan for 7th and 8th-grade students to learn about different types of memory and amnesia. The lesson includes activities such as a working memory game, matching memories to their classifications, and analyzing memory loss in mock medical cases. The lesson aims to help students understand the various forms of memory and the causes of memory problems like amnesia. [Extracted from the article]

The article is devoted to the study of the phenomenon of collective memory in the value contexts of post-modernity. During the 20th century, the culture of memory is revealed through the individual-collective polarity, and in the postmodern era attention is focused on the boundary between them, on the culture of memory in the dimension of the modern media, on the contexts of the global information war. While individual memory loses touch with the past in the dimension of simulated identity, collective memory is usually associated with tradition as a reservoir of memory of the past. Collective memory in the age of modern media is in certain danger of targeted negative external influence, falsification, and inflation. The deepest cultural fears of the 20th century are the deformation or loss of memory, as well as the fear of memory substitution. The main value is linking memory with authenticity in the reproduction of the basic narrative in the cultural practices of today, in which the individual intersects with the collective. That is why the article pays special attention to the border between individual and collective memory, the culture of recall in communicative projects, and the reflection of moral dilemmas in different models of historical memory, the confrontation of different memories. [ABSTRACT FROM AUTHOR]

This article discusses the possibility of practitioners who mistake organic memory loss for dissociative amnesia. It starts with the case of a young man with complete retrograde amnesia due to a traumatic head injury. Because he did not show any gross neurological abnormalities, a neurologist thought his amnesia had a psychological origin. An extensive neuropsychological examination revealed that the man did have an organic reason for his amnesia. Next, the existence of dissociative memory loss as well as isolated organic retrograde amnesia is considered. While cases of organic memory loss are well‐documented, there is hardly any evidence for dissociative amnesia. It is argued that organic memory loss might be mistakenly taken for dissociative amnesia. In line with the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, practitioners are advised to rule out the possibility of organic memory loss, before diagnosing a patient with dissociative amnesia. A patient with autobiographical memory loss but without gross neurological abnormalities may be diagnosed with dissociative amnesia, i.e., amnesia with a psychological origin. In this article, I argue that the absence of apparent neurological symptoms does not mean that a patient's amnesia is caused by psychological factors. Only when a medical history, neuropsychological testing, and brain scans rule out a neurological origin of the memory loss, a patient may genuinely suffer from dissociative amnesia. [ABSTRACT FROM AUTHOR]

• Toll-like receptor 2 (TLR2) recognizes oligomeric tau as a pathogenic ligand. • Oligomeric tau induces inflammatory responses in microglia via TLR2 activation. • Tau-TLR2-mediated microglial activation promotes trans-synaptic tau spread between neurons. • Treatment with anti-TLR2 monoclonal antibody Tomaralimab/OPN-305 ameliorates tau pathology and cognitive function. In Alzheimer's disease, chronic neuroinflammation is accompanied by amyloid and tau pathologies. Especially, aberrant microglial activation is known to precede the regional tau pathology development, but the mechanisms how microglia affect tau spread remain largely unknown. Here, we found that toll-like receptor 2 (TLR2) in microglia recognizes oligomeric tau as a pathogenic ligand and induces inflammatory responses. Knockout of TLR2 reduced tau pathology and microglial activation in rTg4510 tau transgenic mice. Treatment of oligomeric tau induced TLR2 activation and increased inflammatory responses in microglial cells. TLR2 further mediated the tau-induced microglial activation and promoted tau uptake into neurons in neuron-microglia co-culture system and in mouse hippocampus after intracranial tau injection. Importantly, treatment with anti-TLR2 monoclonal antibody Tomaralimab blocked TLR2 activation and inflammatory responses in a dose-dependent manner, and significantly reduced tau spread and memory loss in rTg4510 mice. These results suggest that TLR2 plays a crucial role in tau spread by causing aberrant microglial activation in response to pathological tau, and blocking TLR2 with immunotherapy may ameliorate tau pathogenesis in Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Carbon monoxide (CO) is produced via incomplete combustion of fossil fuels and it may cause long-term neurological sequel upon exposure. Hesperidin (HES), a flavanone glycoside found in citrus plants, exerts diverse beneficial health effects. The present study mechanistically examined the neuroprotective effects of HES in CO-poisoned rats. Thirty male Wistar rats (five groups of six animals) were exposed to 3000 ppm CO for 1 h. Immediately after the exposure and on the next 4 consecutive days (totally five doses), rats intraperitoneally received either normal saline (the control group) or different doses of HES (25, 50, and 100 mg/kg). A sham group that was not exposed to CO was also considered. After evaluation of spatial learning and memory using a Morris water maze (MWM), animals were sacrificed and oxidative stress status in blood samples, and Akt, Bax, Bcl2, and brain-derived neurotrophic factor (BDNF) expression in brain samples were assessed. Western blot analysis indicated increased Akt but decreased Bax/Bcl2 levels in the HES 100 mg/kg, and induced BDNF levels in all HES-treated groups. MWM results showed that HES significantly decreased memory loss. The current findings indicate that HES could alleviate neurological impairments induced by CO in rats. [ABSTRACT FROM AUTHOR]

Objectives: Previous research has noted that a person-centered approach to financial capacity assessment is feasible. This study of personal finance included a review of 12 months of checking account statements followed by research interviews to investigate income, spending, financial literacy, and financial decision-making. The objective of the study was to determine the convergent validity of excess spending to contextual aspects of financial decision-making, financial literacy, and early memory loss. Method: Participants were 114 adults over the age of 60 who came primarily from two research registries; the Healthier Black Elders registry and the Michigan Alzheimer's Disease Research Center registry. After sharing their checking statements participants completed two telephone interviews. Bivariate and multivariate analyses were used to compare those with no memory loss to the memory loss group, and to determine which measures were significantly related to excess spending. Results: There was a significant difference in excess spending between those with early memory loss and those with no memory loss. There was a significant difference in financial decision-making risk scores between the groups, as well as on a memory measure and a financial literacy measure. In a hierarchical regression analysis financial decision-making was the only measure significantly related to excess spending. Conclusion: This study documented the convergent validity of person-centered measures of personal spending and financial decision-making with early memory loss. Early memory loss was related to both excess spending and contextual aspects of financial decision-making. [ABSTRACT FROM AUTHOR]

The aim of this study is to assess the effectiveness of various therapy methods in elderly individuals with traumatic brain injury (TBI), taking into account the degree of memory loss and the severity of the injury. The study was conducted in 2022 in Moscow, Russia, and Sofia, Bulgaria, involving six clinics. A total of 200 elderly patients with TBI participated in the study, with a mean age of 72 years. Patients were categorized into groups based on the degree of memory loss and severity of the injury. Standardized tests, including the Mini‐Mental State Examination (MMSE), Clock Drawing Test, Digit Symbol Substitution Test, and Free, and Cued Selective Reminding Test, were used to assess cognitive functions. The Progressive Learning Test evaluated patients' ability to memorize and reproduce information over time. Groups receiving physical therapy and cognitive rehabilitation showed statistically significant improvement in cognitive functions compared to other therapy methods. Specifically, the mean score of the MMSE in these groups increased by 7 points (p < .001). Patients with more severe memory loss demonstrated more pronounced improvement in cognitive functions following the integrated therapy approach. The mean MMSE score increased by 10 points (p < .001), whereas in patients with milder memory loss, the growth was less significant (mean increase of 5 points, p < .05). Groups receiving physical therapy and cognitive rehabilitation consistently demonstrated significantly better results compared to speech therapy and psychological support throughout the study period. [ABSTRACT FROM AUTHOR]

Background and objectives: As the population of U.S. service members (SMs) who have sustained concussions and more severe traumatic brain injuries (TBIs) during military service ages, understanding the long-term outcomes associated with such injuries will provide critical information that may promote long-term assessment, support, and rehabilitation following military service. The objective of this research was to examine whether concussion and more severe TBIs are associated with greater risk of precursors to dementia (i.e., mild cognitive impairment, memory loss), early-onset dementia, and any dementia. Methods: This study used a retrospective cohort design wherein archival medical and career records from 1980 to 2020 identified U.S. military personnel who retired from military service and their corresponding Tricare-reimbursable medical encounters in inpatient and/or outpatient settings in military treatment facilities and/ or purchased care settings both before and after retirement. All military personnel who served on active duty between 1980 and 2020 and were at least 45 years of age by 2020 were eligible for inclusion (N = 6,092,432). Those who were discharged from military service with a retirement designation, and were thus eligible for Tricare for Life, were included in the analytic sample (N = 1,211,972). Diagnoses of concussion and more severe TBI during active duty service recorded in inpatient settings between 1980 and 2020 and in outpatient settings from 2001 to 2020 were identified. Focal outcomes of interest included memory loss, mild cognitive impairment, Alzheimer's, Lewy Body dementia, frontotemporal dementia, and vascular dementia. Dementia diagnoses before age 65 were labeled early-onset. Results: Those with (vs. without) concussion diagnoses during military service were significantly more likely to be diagnosed with memory loss and mild cognitive impairment and any of the dementias examined. However, they were not at greater risk of being diagnosed with early-onset dementia. Discussion: Military SMs diagnosed with concussion may be at elevated risk for long-term neurodegenerative outcomes including memory loss, mild cognitive impairment, and dementia. As the population of SMs who sustained TBI during the Global War on Terror continue to age, the prevalence of dementia will increase and may bring a unique burden to the VHA. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is one of the most common neurodegenerative disorders and is characterized by a decrease in learning capacity, memory loss and behavioral changes. In addition to the well-recognized amyloid-β cascade hypothesis and hyperphosphorylated Tau hypothesis, accumulating evidence has led to the proposal of the mitochondrial dysfunction hypothesis as the primary etiology of AD. However, the predominant molecular mechanisms underlying the development and progression of AD have not been fully elucidated. Mitochondrial dysfunction is not only considered an early event in AD pathogenesis but is also involved in the whole course of the disease, with numerous pathophysiological processes, including disordered energy metabolism, Ca2+ homeostasis dysfunction and hyperactive oxidative stress. In the current review, we have integrated emerging evidence to summarize the main mitochondrial alterations— bioenergetic metabolism, mitochondrial inheritance, mitobiogenesis, fission– fusion dynamics, mitochondrial degradation, and mitochondrial movement— underlying AD pathogenesis; precisely identified the mitochondrial regulators; discussed the potential mechanisms and primary processes; highlighted the leading players; and noted additional incidental signaling pathway changes. This review may help to stimulate research exploring mitochondrial metabolically-oriented neuroprotection strategies in AD therapies, leading to a better understanding of the link between the mitochondrial dysfunction hypothesis and AD pathogenesis. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is the most common cause of dementia, characterized by memory loss, cognitive decline, personality changes, and various neurological symptoms. The role of blood–brain barrier (BBB) injury, extracellular matrix (ECM) abnormalities, and oligodendrocytes (ODCs) dysfunction in AD has gained increasing attention, yet the detailed pathogenesis remains elusive. This study integrates single-cell sequencing of AD patients' cerebrovascular system with a genome-wide association analysis. It aims to elucidate the associations and potential mechanisms behind pericytes injury, ECM disorder, and ODCs dysfunction in AD pathogenesis. Finally, we identified that abnormalities in the pericyte PI3K–AKT–FOXO signaling pathway may be involved in the pathogenic process of AD. This comprehensive approach sheds new light on the complex etiology of AD and opens avenues for advanced research into its pathogenesis and therapeutic strategies. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a brain illness that causes gradual memory loss. AD has no treatment and cannot be cured, so early detection is critical. Various AD diagnosis approaches are used in this regard, but Magnetic Resonance Imaging (MRI) provides the most helpful neuroimaging tool for detecting AD. In this paper, we employ a DenseNet-201 based transfer learning technique for diagnosing different Alzheimer's stages as Non-Demented (ND), Moderate Demented (MOD), Mild Demented (MD), Very Mild Demented (VMD), and Severe Demented (SD). The suggested method for a dataset of MRI scans for Alzheimer's disease is divided into five classes. Data augmentation methods were used to expand the size of the dataset and increase DenseNet-201's accuracy. It was found that the proposed strategy provides a very high classification accuracy. This practical and reliable model delivers a success rate of 98.24%. The findings of the experiments demonstrate that the suggested deep learning approach is more accurate and performs well compared to existing techniques and state-of-the-art methods. [ABSTRACT FROM AUTHOR]

Background: Reduction of adult hippocampal neurogenesis is an early critical event in Alzheimer's disease (AD), contributing to progressive memory loss and cognitive decline. Reduced levels of the nucleoporin 153 (Nup153), a key epigenetic regulator of NSC stemness, characterize the neural stem cells isolated from a mouse model of AD (3×Tg) (AD-NSCs) and determine their altered plasticity and gene expression. Methods: Nup153-regulated mechanisms contributing to NSC function were investigated: (1) in cultured NSCs isolated from AD and wild type (WT) mice by proteomics; (2) in vivo by lentiviral-mediated delivery of Nup153 or GFP in the hippocampus of AD and control mice analyzing neurogenesis and cognitive function; (3) in human iPSC-derived brain organoids obtained from AD patients and control subjects as a model of neurodevelopment. Results: Proteomic approach identified Nup153 interactors in WT- and AD-NSCs potentially implicated in neurogenesis regulation. Gene ontology (GO) analysis showed that Nup153-bound proteins in WT-NSCs were involved in RNA metabolism, nuclear import and epigenetic mechanisms. Nup153-bound proteins in AD-NSCs were involved in pathways of neurodegeneration, mitochondrial dysfunction, proteasomal processing and RNA degradation. Furthermore, recovery of Nup153 levels in AD-NSCs reduced the levels of oxidative stress markers and recovered proteasomal activity. Lentiviral-mediated delivery of Nup153 in the hippocampal niche of AD mice increased the proliferation of early progenitors, marked by BrdU/DCX and BrdU/PSANCAM positivity and, later, the integration of differentiating neurons in the cell granule layer (BrdU/NeuN+ cells) compared with GFP-injected AD mice. Consistently, Nup153-injected AD mice showed an improvement of cognitive performance in comparison to AD-GFP mice at 1 month after virus delivery assessed by Morris Water Maze. To validate the role of Nup153 in neurogenesis we took advantage of brain organoids derived from AD-iPSCs characterized by fewer neuroepithelial progenitor loops and reduced differentiation areas. The upregulation of Nup153 in AD organoids recovered the formation of neural-like tubes and differentiation. Conclusions: Our data suggest that the positive effect of Nup153 on neurogenesis is based on a complex regulatory network orchestrated by Nup153 and that this protein is a valuable disease target. [ABSTRACT FROM AUTHOR]

Congressional staff serve as the "invisible force" in Congress by helping draft legislation and conduct oversight. Given this, excessive turnover among staff is a loss of institutional memory and inhibits legislators' ability to effectively conduct their constitutional duties. Using a mixed methods research design of interviews and a new survey of staff in the 115th session of Congress, I capture staffer intent to leave their current position and track whether they actually left their position 12 months later. Similar to civil servants, staff who report dissatisfaction with coworkers report higher levels of turnover intention, while the type of office, age, and level of education impact actual turnover. However, the extent to which polarization impacts staffers' job satisfaction impacts both intention and actual exit. My study makes a unique contributions to the growing body of literature devoted to understanding congressional staff by providing important insights into how to recruit and retain staff. [ABSTRACT FROM AUTHOR]

Nonreciprocal magnetotransport is one of the central topics in spintronics because of its importance for electrically probing magnetic information. Among numerous electrical probes used to read magnetic orders, unidirectional magnetoresistance (UMR), characterized by sign changes upon reversal of either current or magnetization, is currently a matter of great interest and has been identified in various spin–orbit-coupled bilayer systems composed of an (anti)ferromagnetic layer and a nonmagnetic layer with strong spin Hall effect. A recent theoretical work predicts that a spin-anomalous-Hall (SAH) UMR in those metallic conducting bilayers can originate from the spin-anomalous-Hall effect of the ferromagnetic layer and the structural inversion asymmetry. However, this type of UMR has not been reported experimentally. Here, we give the experimental evidence of spin-anomalous-Hall UMR in the light-metal/ferromagnetic-metal Cu/Co bilayers, where the emergence of net nonequilibrium spin density is attributed to the interfacial spin leakage asymmetry due to the spin memory loss effect at the Cu/Co interface and multiple spin reflections. We also show a highly tunable UMR in the Cu/Co/CuOx trilayer by varying the Cu thickness, which is due to the competition between the orbital Rashba effect in Co/CuOx and the spin-anomalous-Hall effect in Cu/Co. Our work widens the material choice for UMR device applications and provides an alternative approach to detect in-plane magnetization without an external spin polarizer. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a progressive degenerative disorder that causes behavioral changes, cognitive decline, and memory loss. Currently, AD is incurable, and the few available medicines may, at best, improve symptoms or slow down AD progression. One main challenge in drug delivery to the brain is the presence of the blood–brain barrier (BBB), a semi-permeable layer around cerebral capillaries controlling the influx of blood-borne particles into the brain. In this paper, a mathematical model of drug transport to the brain is proposed that incorporates two mechanisms of BBB crossing: transcytosis and diffusion. To account for the structural damage and accumulation of harmful waste in the brain caused by AD, the diffusion is assumed to be anomalous and is modeled using spatial Riemann–Liouville fractional-order derivatives. The model's parameters are taken from published experimental observations of the delivery to mice brains of the orally administered AD drug donepezil hydrochloride. Numerical simulations suggest that drug delivery modalities should depend on the BBB fitness and anomalous diffusion and be tailored to AD severity. These results may inspire novel brain-targeted drug carriers for improved AD therapies. [ABSTRACT FROM AUTHOR]

Long-lasting COVID-19 (long COVID) diseases constitute a real life-changing burden for many patients around the globe and, overall, can be considered societal and economic issues. They include a variety of symptoms, such as fatigue, loss of smell (anosmia), and neurological–cognitive sequelae, such as memory loss, anxiety, brain fog, acute encephalitis, and stroke, collectively called long neuro-COVID-19 (long neuro-COVID). They also include cardiopulmonary sequelae, such as myocardial infarction, pulmonary damage, fibrosis, gastrointestinal dysregulation, renal failure, and vascular endothelial dysregulation, and the onset of new diabetes, with each symptom usually being treated individually. The main unmet challenge is to understand the mechanisms of the pathophysiologic sequelae, in particular the neurological symptoms. This mini-review presents the main mechanistic hypotheses considered to explain the multiple long neuro-COVID symptoms, namely immune dysregulation and prolonged inflammation, persistent viral reservoirs, vascular and endothelial dysfunction, and the disruption of the neurotransmitter signaling along various paths. We suggest that the nucleoprotein N of SARS-CoV-2 constitutes a "hub" between the virus and the host inflammation, immunity, and neurotransmission. [ABSTRACT FROM AUTHOR]

Objective Autoimmune encephalitis includes a heterogeneous group of rare and complex diseases, usually presenting with severe and disabling symptoms, such as behavioral changes, cognitive deficits, and seizures. Method This report presents the case of a 26-year-old man who was diagnosed with autoimmune encephalitis following SARS-CoV-2 vaccination (<40 days). Symptoms first appeared in February 2022 with a temporal seizure, associated with confusion and memory loss. Psychiatric manifestations such as disorientation and altered thought contents emerged soon after. Results Neuroimaging testing showed signs of hypometabolism in occipital, prefrontal, and temporal regions, whereas an extensive neuropsychological assessment revealed the presence of multiple alterations in memory, executive, and visuoconstructive processes. Conclusions In this case, a combination of neuroimaging testing, psychiatric evaluation, and neuropsychological assessment provided evidence for a diagnosis of autoimmune encephalitis post-vaccination. Early recognition is essential in order to prevent clinical progression; avoid intractable epilepsy, brain atrophy, and cognitive impairment; and improve prognosis. [ABSTRACT FROM AUTHOR]

Copyright of Psychological Science is the property of Psychological Science Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Consistent long-term exercise has been understood to have broad positive effects on overall cognition, and there is also evidence supporting the benefits of exercise on episodic memory in particular. However, different forms of exercise, such as aerobic and resistance, can induce different physiological implications, changing the ways in which episodic memory is affected. This review paper aimed to investigate the ways and degrees to which different forms of long-term aerobic and resistance exercise affect episodic memory, as well as investigate the role that age plays in the magnitude of this effect. While both resistance and aerobic training were likely to illustrate an improvement in episodic memory performance, the results of long-term aerobic training were expected to have a greater positive impact on episodic memory. It was also expected that age would have a direct correlation on the magnitude of this effect. These hypotheses were supported by the findings of the review. Episodic memory likely experiences greatest improvement through exercise-induced neurogenesis and signalling pathways activated by increased levels of Brain-Derived Neurotrophic Factor (BDNF) and Insulin-like Growth Factor-1 (IGF-1), primarily as a result of aerobic and resistance exercise, respectively. Furthermore, it was found that the magnitude of this effect peaked within the age range of 55-68 years, potentially supporting the existence of a more exact optimal age for which exercise would have the most pronounced effect on episodic memory. Understanding the effect of both long-term aerobic and resistance training on episodic memory can have a widespread impact. It can unlock avenues to potentially enhancing memory and may help discover new methods to treat or prevent cognitive decline and neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

MDD often brings about numerous health challenges and disruptions, with memory loss emerging as a prominent concern. Many studies have tried to find the relationship between MDD and the patients' memory functions. Research has shown that depression affects memory encoding in a variety of significant ways. This paper analyzes research articles and relevant literature from 2000 to 2023 to connect the effects of depression to symptoms of memory loss. The included studies cover the effects on various types of memory encoding for patients either under depression or in remitted depression throughout differing age cohorts. Research methods include testing on source memory, RCFT (Rey-Osterrieth-Complex-Figure-Test), and learning and recall. Overall, depression leads to many negative effects on retention even when a patient is in remission including deficits in contextual cognitive memory, both verbal and non-verbal memory, and working memory. Depression patients have difficulties during the encoding process, which causes impairments of these memories. Giving patients extra cognitive support can help lessen the deficits. However, the problem alters with aging, memory kinds, the number of past depressive episodes, and other control factors. [ABSTRACT FROM AUTHOR]

This article investigates elements of empathy in the Zhuangzi 莊子. It outlines four prominent aspects of current scholarship on empathy: different types of empathy, the other-centeredness of empathy, empathy as a process and the role empathy plays in responsiveness to others, and interaction between empathy and other capacities. Based on materials from the Zhuangzi that involve elements of empathy, I delegate them respectively to these four areas. While the Zhuangzi does not invent any specific term for an exclusive designation of the meaning of empathy, I attempt to show that the Zhuangzi does explore the phenomena of empathy to a great extent. It characterizes unique features of empathy, such as other-centeredness, perceptual directness, its function as listening, mirroring, qi 氣-connecting and receptivity, the issue of how to cultivate one's empathic capacity in the everyday encounter with others, and especially how empathic capacity works closely with the Zhuangzian forgetfulness of oneself. [ABSTRACT FROM AUTHOR]

Copyright of Boletín Latinoamericano y del Caribe de Plantas Medicinales y Aromáticas is the property of Universidad de Santiago de Chile and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Population aging is a global reality driven by increased life expectancy. This demographic phenomenon is intrinsically linked to the epidemic of cognitive disorders such as dementia and Alzheimer's disease, posing challenges for elderly and their families. In this context, the search for new therapeutic strategies to prevent or minimize cognitive impairments becomes urgent, as these deficits are primarily associated with oxidative damage and increased neuroinflammation. Ferulic acid (FA), a natural and potent antioxidant compound, is proposed to be nanoencapsulated to target the central nervous system effectively with lower doses and an extended duration of action. Here, we evaluated the effects of the nanoencapsulated FA on d-galactose (d-Gal)- induced memory impairments. Male Wistar adult rats were treated with ferulic acid-loaded nanocapsules (FA-Nc) or non-encapsulated ferulic acid (D-FA) for 8 weeks concurrently with d-Gal (150 mg/kg s.c.) injection. As expected, our findings showed that d-Gal injection impaired memory processes and increased anxiety behavior, whereas FA-Nc treatment ameliorated these behavioral impairments associated with the aging process induced by d-Gal. At the molecular level, nanoencapsulated ferulic acid (FA-Nc) ameliorated the decrease in ACh and glutamate induced by d-galactose (d-Gal), and also increased GABA levels in the dorsal hippocampus, indicating its therapeutic superiority. Additional studies are needed to elucidate the mechanisms underlying our current promising outcomes. Nanoscience applied to pharmacology can reduce drug dosage, thereby minimizing adverse effects while enhancing therapeutic response, particularly in neurodegenerative diseases associated with aging. Therefore, the strategy of brain-targeted drug delivery through nanoencapsulation can be effective in mitigating aging-related factors that may lead to cognitive deficits. [ABSTRACT FROM AUTHOR]

Alzheimer´s disease (AD) stands out as the most common chronic neurodegenerative disorder. AD is characterized by progressive cognitive decline and memory loss, with neurodegeneration as its primary pathological feature. The role of neuroinflammation in the disease course has become a focus of intense research. While microglia, the brain's resident macrophages, have been pivotal to study central immune inflammation, recent evidence underscores the contributions of other cellular entities to the neuroinflammatory process. In this article, we review the inflammatory role of microglia and astrocytes, focusing on their interactions with AD's core pathologies, amyloid beta deposition, and tau tangle formation. Additionally, we also discuss how different modes of regulated cell death in AD may impact the chronic neuroinflammatory environment. This review aims to highlight the evolving landscape of neuroinflammatory research in AD and underscores the importance of considering multiple cellular contributors when developing new therapeutic strategies. [ABSTRACT FROM AUTHOR]

This work investigates the interplay between interfacial spin–orbit coupling (SOC) and magnon excitation-induced spin memory loss in epitaxial L10-FePt/MgO/L10-FePt magnetic tunnel junctions, which is crucial for advancing spintronic technologies. By employing systematic temperature-dependent transport measurements and inelastic electron tunneling spectroscopy, our study reveals that interfacial SOC at the Pt-terminated FePt/MgO interface significantly enhances magnon excitation during electron tunneling. This process results in a pronounced loss of spin memory in the spin-polarized current, diminishing the tunnel magnetoresistance ratio. Our findings provide critical insights into the mechanisms of spin memory loss, offering directions for optimizing spintronic device performance in the context of pronounced SOC environments. [ABSTRACT FROM AUTHOR]

Background: Cognitive dysfunction caused by infection frequently emerges as a complication in sepsis survivor patients. However, a comprehensive understanding of its pathogenesis remains elusive. Methods: In our in vivo experiments, an animal model of endotoxemia was employed, utilizing the Novel Object Recognition Test and Morris Water Maze Test to assess cognitive function. Various techniques, including immunofluorescent staining, Western blotting, blood‒brain barrier permeability assessment, Limulus Amebocyte Lysate (LAL) assay, and Proximity-ligation assay, were employed to identify brain pathological injury and neuroinflammation. To discern the role of Caspase-11 (Casp11) in hematopoietic or non-hematopoietic cells in endotoxemia-induced cognitive decline, bone marrow chimeras were generated through bone marrow transplantation (BMT) using wild-type (WT) and Casp11-deficient mice. In vitro studies involved treating BV2 cells with E. coli-derived outer membrane vesicles to mimic in vivo conditions. Results: Our findings indicate that the deficiency of Casp11-GSDMD signaling pathways reverses infection-induced cognitive dysfunction. Moreover, cognitive dysfunction can be ameliorated by blocking the IL-1 effect. Mechanistically, the absence of Casp11 signaling significantly mitigated blood‒brain barrier leakage, microglial activation, and synaptic damage in the hippocampal CA3 region, ultimately leading to improved cognitive function. Conclusion: This study unveils the crucial contribution of Casp11 and GSDMD to cognitive impairments and spatial memory loss in a murine sepsis model. Targeting Casp11 signaling emerges as a promising strategy for preventing or treating cognitive dysfunction in patients with severe infections. [ABSTRACT FROM AUTHOR]

Extracellular matrix (ECM) remodeling is strongly linked to Alzheimer's disease (AD) risk; however, the underlying mechanisms are not fully understood. Here, it is found that the injection of chondroitinase ABC (ChABC), mimicking ECM remodeling, into the medial prefrontal cortex (mPFC) reversed short‐term memory loss and reduced amyloid‐beta (Aβ) deposition in 5xFAD mice. ECM remodeling also reactivated astrocytes, reduced the levels of aggrecan in Aβ plaques, and enhanced astrocyte recruitment to surrounding plaques. Importantly, ECM remodeling enhanced the autophagy‐lysosome pathway in astrocytes, thereby mediating Aβ clearance and alleviating AD pathology. ECM remodeling also promoted Aβ plaque phagocytosis by astrocytes by activating the astrocytic phagocytosis receptor MERTK and promoting astrocytic vesicle circulation. The study identified a cellular mechanism in which ECM remodeling activates the astrocytic autophagy‐lysosomal pathway and alleviates AD pathology. Targeting ECM remodeling may represent a potential therapeutic strategy for AD and serve as a reference for the treatment of this disease. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to evaluate and compare the diagnostic capacity of five cognitive screening tests for the diagnosis of mild cognitive impairment (MCI) in patients consulting by memory loss. Methods: A cross-sectional study involving 140 participants with a mean age of 74.42 ± 7.60 years, 87 (62.14%) women. Patients were classified as MCI or cognitively unimpaired according to a comprehensive neuropsychological battery. The diagnostic properties of the following screening tests were compared: Mini-Mental State Examination (MMSE), Addenbrooke's Cognitive Examination III (ACE-III) and Mini-Addenbrooke (M-ACE), Memory Impairment Screen (MIS), Montreal Cognitive Assessment (MoCA), and Rowland Universal Dementia Assessment Scale (RUDAS). Results: The area under the curve (AUC) was 0.861 for the ACE-III, 0.867 for M-ACE, 0.791 for MoCA, 0.795 for MMSE, 0.731 for RUDAS, and 0.672 for MIS. For the memory components, the AUC was 0.869 for ACE-III, 0.717 for MMSE, 0.755 for MoCA, and 0.720 for RUDAS. Cronbach's alpha was 0.827 for ACE-III, 0.505 for MMSE, 0.896 for MoCA, and 0.721 for RUDAS. Correlations with Free and Cued Selective Reminding Test were moderate with M-ACE, ACE-III, and MoCA, and moderate for the other tests. The M-ACE showed the best balance between diagnostic capacity and time of administration. Conclusions: ACE-III and its brief version M-ACE showed better diagnostic properties for the diagnosis of MCI than the other screening tests. MoCA and MMSE showed adequate properties, while the diagnostic capacity of MIS and RUDAS was limited. [ABSTRACT FROM AUTHOR]

Background: Research suggests that the neighborhood in which people live can be a risk or protective factor for various health outcomes, including cognitive decline to Alzheimer's disease. Similar to the impact of neighborhood on health outcomes, sleep difficulties have been linked to cognitive function in older adults. However, few studies have examined how neighborhood physical disorders moderate the effects of sleep on subjective cognitive decline (SCD). Objective: The study examined the moderating effect of neighborhood factors on the relationship between sleep difficulties and SCD. Methods: Data were obtained from 2,494 respondents (1,065 males and 1,429 females) from Wave 11 of the National Health and Aging Trends (NHATS) data. Sleep difficulties were operationalized as the presence of difficulties in falling and staying asleep. Neighborhood physical disorder (e.g., vandalism, graffiti) was based on interviewer observations of respondents' neighborhoods. SCD was operationalized as subjective reports of increasing or worse memory loss in the past 12 months and present memory rating. We utilized Linear regression to test neighborhood physical disorder as a moderator of the relationship between sleep difficulties and SCD. Results: We found a significant interaction between sleep difficulties and neighborhood physical disorder on SCD (β=0.046, p = 0.031, 95% CI[0.00,0.51], p < 0.001). Participants who reported higher average sleep difficulties and higher levels of neighborhood physical disorder were more likely to report SCD. Conclusions: Our findings add to inform future health interventions and policy recommendations that address modifiable sources of cognitive decline and risk of Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is characterized by, among other things, dementia and a decline in cognitive performance. In AD, dementia has neurodegenerative features and starts with mild cognitive impairment (MCI). Research indicates that apoptosis and neuronal loss occur in AD, in which oxidative stress plays an important role. Therefore, reducing oxidative stress with antioxidants is a natural strategy to prevent and slow down the progression of AD. Carotenoids are natural pigments commonly found in fruits and vegetables. They include lipophilic carotenes, such as lycopene, α- and β-carotenes, and more polar xanthophylls, for example, lutein, zeaxanthin, canthaxanthin, and β-cryptoxanthin. Carotenoids can cross the blood–brain barrier (BBB) and scavenge free radicals, especially singlet oxygen, which helps prevent the peroxidation of lipids abundant in the brain. As a result, carotenoids have neuroprotective potential. Numerous in vivo and in vitro studies, as well as randomized controlled trials, have mostly confirmed that carotenoids can help prevent neurodegeneration and alleviate cognitive impairment in AD. While carotenoids have not been officially approved as an AD therapy, they are indicated in the diet recommended for AD, including the consumption of products rich in carotenoids. This review summarizes the latest research findings supporting the potential use of carotenoids in preventing and alleviating AD symptoms. A literature review suggests that a diet rich in carotenoids should be promoted to avoid cognitive decline in AD. One of the goals of the food industry should be to encourage the enrichment of food products with functional substances, such as carotenoids, which may reduce the risk of neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

AbstractThis study explores the experiences of fathers of existing children following pregnancy loss. Participants were 12 Israeli men who experienced pregnancy loss and had other children at the time. Semi-structured interviews were conducted. Four themes were generated through thematic analysis. The first was “emotional reactions”: fathers described emotional disengagement after the loss. The second was “taking on a functional role”: fathers assumed a functional role as supporters in their familial relationships. The third was “acknowledged at home but disenfranchised elsewhere”: fathers felt their grief was unacknowledged by people around them. The fourth was “the relationship with the baby”: fathers struggled to define the loss. They were able to connect with memories and pain of the loss through their re-engagement with their other children. Findings suggest that fathers feel grief that is disenfranchized by society. These findings highlight a need for individual and group interventions to support fathers in their grief. [ABSTRACT FROM AUTHOR]

Time-restricted feeding (RF) is known to shift the phasing of gene expression in most primary metabolic tissues, whereas a time misalignment between the suprachiasmatic nucleus circadian clock (SCNCC) and its peripheral CCs (PCC's) is known to induce various pathophysiological conditions, including a metabolic syndrome. We now report that a unique "light therapy," involving different light intensities (TZT0-ZT12150-TZT0-ZT12700 lx, TZT0-ZT1275-TZT0-ZT12150 lx, and TZT0-ZT12350-TZT0-ZT12700 lx), realigns the RF-generated misalignment between the SCNCC and the PCC's. Using such high-light regime, we show that through shifting the SCNCC and its activity, it is possible in a RF and "night-shifted mouse model" to prevent/correct pathophysiologies (e.g., a metabolic syndrome, a loss of memory, cardiovascular abnormalities). Our data indicate that such a "high-light regime" could be used as a unique chronotherapy, for those working on night shifts or suffering from jet-lag, in order to realign their SCNCC and PCC's, thereby preventing the generation of pathophysiological conditions. [ABSTRACT FROM AUTHOR]

Cognitive problems like Dementia and Alzheimer’s are usually challenging to diagnose but can be noticed by some signs of their symptoms. The most common symptoms are confusion, trouble finding the right word, memory loss, and difficulty concentrating. This study aims to design a cognitive activity detection and tracing system that contains games and analyzes users’ performances then displays detailed statistics to the users. The proposed Cognitive Activity Detection and Tracing System (CADTS) is software that contains different kinds of games from different categories inside its body that aims to measure cognitive activity by utilizing formulations in the context of the games and give feedback to users concerning the performance analyses done. The purpose of these analyses is to catch the signs of symptoms. An insight into a possible scoring system is provided, and as our results, several descriptive statistics are shared based on the tests conducted. [ABSTRACT FROM AUTHOR]

Early pathological upregulation of adenosine A2A receptors (A2ARs), one of the caffeine targets, by neurons is thought to be involved in the development of synaptic and memory deficits in Alzheimer's disease (AD) but mechanisms remain ill-defined. To tackle this question, we promoted a neuronal upregulation of A2AR in the hippocampus of APP/PS1 mice developing AD-like amyloidogenesis. Our findings revealed that the early upregulation of A2AR in the presence of an ongoing amyloid pathology exacerbates memory impairments of APP/PS1 mice. These behavioural changes were not linked to major change in the development of amyloid pathology but rather associated with increased phosphorylated tau at neuritic plaques. Moreover, proteomic and transcriptomic analyses coupled with quantitative immunofluorescence studies indicated that neuronal upregulation of the receptor promoted both neuronal and non-neuronal autonomous alterations, i.e. enhanced neuroinflammatory response but also loss of excitatory synapses and impaired neuronal mitochondrial function, presumably accounting for the detrimental effect on memory. Overall, our results provide compelling evidence that neuronal A2AR dysfunction, as seen in the brain of patients, contributes to amyloid-related pathogenesis and underscores the potential of A2AR as a relevant therapeutic target for mitigating cognitive impairments in this neurodegenerative disorder. [ABSTRACT FROM AUTHOR]

Purpose: Memory plays an essential role in daily life and is one of the first functions to deteriorate in cognitive impairment and dementia. Transcutaneous vagus nerve stimulation (tVNS) is a promising therapeutic method; however, its ability to enhance memory is underexplored, especially considering long-term stimulation. We aimed to investigate the effect of a 2-week course of auricular tVNS (taVNS) on memory in a non-clinical population. Methods: This single-blind randomized placebo-wait-list controlled trial recruited 76 participants (30 men; mean age 48.32 years) and randomized them into four groups: early active/sham taVNS and late active/sham taVNS. Participation in the study lasted 4 weeks; early groups underwent 2 weeks intervention immediately following the first study site visit (days 0–13) and late groups 2 weeks after the first study site visit (days 14–27). Active and sham taVNS included 2 weeks of daily 4-h neurostimulation at the tragus or earlobe, respectively. To assess memory, we used the Rey Auditory Verbal Learning Test. Results: Two weeks of active taVNS, but not sham taVNS, improved immediate recall and short-term memory score both in early and late groups. Furthermore, the improvements persisted over subsequent follow-up in early active taVNS. Importantly, the effect of active taVNS was superior to sham for immediate recall in both early and late groups. There were no statistical differences in delayed recall. Conclusion: Our findings suggest that taVNS has potential to improve memory, particularly immediate recall, and may be an effective method in preventing memory loss and mitigating cognitive aging. [ABSTRACT FROM AUTHOR]

Objective; Oxidative stress results in neuronal degeneration leading to cognitive decline. Microglia in brain tissue produces reactive oxygen species (ROS), which modulate synaptic communication between neurons. ROS can lead to neuroinflammation, which can cause neurodegeneration and memory loss. Talinum triangulare was investigated for its cognitive, anti-oxidative and anti-inflammatory potentials in male wistar rats. Materials and methods; 25 adult female rats weighing between 150 g–200 g were grouped (n = 5) into Group 1 (control group) received 1 mL/kg of distilled water, group 2–5 were administered with 100 mg/kg, 200 mg/kg and 400 mg/kg T. triangulare methanol extract and 2.5 mg/kg donepezil, 100 mg/kg cadmium respectively via oral gavage. The administration lasted for 21 days and neuro behavioural parameters, biochemical and histological analysis of the hippocampus were evaluated. The assessment of spatial learning and memory was evaluated using Classic labyrinth task. Results; There was significantly (p < 0.05) reduced escape time latency and increased time latency in the probe trial in Morris water maze; and reduced time latency in the labyrinth by T. triangulare methanol extract (100, 200 and 400 mg/kg) compared with the control and cadmium treated groups. T. triangulare methanol extract and donepezil significantly (p < 0.05) reduced acetylcholinesterase (AChE), tissue necrosis factor-α (TNF-α), interleukin-6 (IL-6) activities and significantly (p < 0.05) increased gluthathione peroxidase activity (GPx) and catalase (CAT) respectively. Conclusion; These findings revealed that T. triangulare methanol extract enhanced cognitive function and exhibited anti-oxidative and anti-inflammatory potentials. [ABSTRACT FROM AUTHOR]

The etiology of brain fog associated with long COVID is not clear. Based on some preliminary work, disruption of the blood-brain barrier has been hypothesized, but has not been tested in patients with long COVID. In this case-control pilot study, we evaluated blood-brain barrier permeability in patients with long COVID and subjective memory loss or brain fog. We used 99 m Technetium diethylenetriaminepentaacetic acid single-photon emission computed tomography (SPECT) to measure blood-brain barrier permeability and a telephone assessment (T-cog) to measure cognitive function. The blood-brain barrier permeability was quantified via SPECT standard uptake value (SUV). We assessed the blood-brain barrier permeability in 14 long COVID patients and 10 control participants without subjective cognitive impairment or brain fog. Participants in the two groups were similar in age. The long COVID group had more comorbidities compared to the control group. There was no difference in the SUVs in the long COVID (0.22 ± 0.12) vs the control (0.17 ± 0.04) group. There was no difference in the T-cog results in the two groups either. We found no evidence of a difference in blood-brain permeability in patients with long COVID when compared to controls without a known history of COVID-19 infection. Larger studies are needed to confirm these findings. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory loss and cognitive impairment. It severely affects the quality of life of victims. The prevalence of AD has been increasing in recent years. Therefore, it is of great importance to elucidate the pathogenic mechanism of AD and search for effective therapeutic approaches. Gut microbiota dysbiosis, an altered state of gut microbiota, has been well known for its involvement in the pathogenesis of AD. Much effort has been made in searching for approaches capable of modulating the composition of gut microbiota in recent years. Herbal medicines have attracted extensive attention in recent decades for the prevention and treatment of AD. Here, we gave an overview of the recent research progress on the modulatory effects of herbal medicines and herbal formulae on gut microbiota as well as the possible beneficial effects on AD, which may provide new insights into the discovery of anti-AD agents and their therapeutic potential for AD through modulating the composition of gut microbiota. [ABSTRACT FROM AUTHOR]

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This study investigates whether Andrographolide-loaded Lactose β-Cyclodextrin (ALN-βCD) nanoparticles enhance cognitive function, particularly spatial learning and memory. The successful conjugation of lactose to β-cyclodextrin was confirmed via 1H NMR spectroscopy, facilitating neuronal cell entry. The solvent evaporation method was used to create the nanoparticles, which were characterised for particle size, PDI, zeta potential, and drug release. The nanoparticles exhibited a size of 247.9 ± 3.2 nm, a PDI of 0.5 ± 0.02, and a zeta potential of 26.8 ± 2.5 mV. FTIR and TEM analyses, along with in vitro drug release and BBB permeability studies, confirmed their stability and efficacy. Behavioural tests, including the Elevated Plus Maze, Y-Maze, Object Recognition, and Locomotor Activity tests, demonstrated significant improvements in memory, motor coordination, and exploration time in the nanoparticle-treated groups. The group treated with ALN-βCD at a dose of 100 mg/kg/p.o. showed superior cognitive performance compared to the group receiving free andrographolides (AG). Biochemical assays indicated a significant reduction in acetylcholinesterase activity and lipid peroxidation, suggesting increased acetylcholine levels and reduced oxidative stress. Histopathological examination showed improved neuronal function without toxicity. The results showed significant improvements (p < 0.001) in memory and cognitive abilities in experimental animals, highlighting the potential of ALN-βCD nanoparticles as a non-invasive treatment for memory loss. These promising findings warrant further exploration through clinical trials. [ABSTRACT FROM AUTHOR]

This article presents a brief, constructive, theological account of memory in response to contemporary questions regarding memory loss via Augustine's account of memory, which elucidates the remembering subject's openness and relatedness to God and the communion of saints. First, I examine Augustine's Confessions, showing how memory is embodied, affective, and cogitative, and that memory's end is in relation to God and the communion of saints. Afterwards, I consider the resonances between Augustine's account of memory and two threads of research in dementia studies—namely, the notion of the 'embodied self' and the concept of memory 'extension'—in order to propose how such a reading of Augustine on memory might contribute towards theological accounts and responses to memory impairment or loss. [ABSTRACT FROM AUTHOR]

Brain pathological changes impair cognition early in disease etiology. There is an urgent need to understand aging-linked mechanisms of early memory loss to develop therapeutic strategies and prevent the development of cognitive impairment. Tusc2 is a mitochondrial-resident protein regulating Ca2+ fluxes to and from mitochondria impacting overall health. We previously reported that Tusc2−/− female mice develop chronic inflammation and age prematurely, causing age- and sex-dependent spatial memory deficits at 5 months old. Therefore, we investigated Tusc2-dependent mechanisms of memory impairment in 4-month-old mice, comparing changes in resident and brain-infiltrating immune cells. Interestingly, Tusc2−/− female mice demonstrated a pro-inflammatory increase in astrocytes, expression of IFN-γ in CD4+ T cells and Granzyme-B in CD8+T cells. We also found fewer FOXP3+ T-regulatory cells and Ly49G+ NK and Ly49G+ NKT cells in female Tusc2−/− brains, suggesting a dampened anti-inflammatory response. Moreover, Tusc2−/− hippocampi exhibited Tusc2- and sex-specific protein changes associated with brain plasticity, including mTOR activation, and Calbindin and CamKII dysregulation affecting intracellular Ca2+ dynamics. Overall, the data suggest that dysregulation of Ca2+-dependent processes and a heightened pro-inflammatory brain microenvironment in Tusc2−/− mice could underlie cognitive impairment. Thus, strategies to modulate the mitochondrial Tusc2- and Ca2+- signaling pathways in the brain should be explored to improve cognitive health. [ABSTRACT FROM AUTHOR]