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JAMA Network Open Nov 2023Despite existing federal programs to increase access to food, food insecurity is common among US older adults. Food insecurity may affect Alzheimer disease and Alzheimer...
IMPORTANCE
Despite existing federal programs to increase access to food, food insecurity is common among US older adults. Food insecurity may affect Alzheimer disease and Alzheimer disease-related dementias via multiple mechanisms, yet there is almost no quantitative research evaluating this association.
OBJECTIVE
To examine whether food insecurity in older adults is associated with later-life cognitive outcomes.
DESIGN, SETTING, AND PARTICIPANTS
This cohort study of US residents aged 50 years and older from the US Health and Retirement Study was restricted to respondents with food insecurity data in 2013 and cognitive outcome data between calendar years 2014 and 2018. Analyses were conducted from June 1 to September 22, 2023.
EXPOSURE
Food insecurity status in 2013 was assessed using the validated US Department of Agriculture 6-item Household Food Security Module. Respondents were classified as being food secure, low food secure, and very low food secure.
MAIN OUTCOMES AND MEASURES
Outcomes were dementia probability and memory score (standardized to 1998 units), estimated biennially between 2014 and 2018 using a previously validated algorithm. Generalized estimation equations were fit for dementia risk and linear mixed-effects models for memory score, taking selective attrition into account through inverse probability of censoring weights.
RESULTS
The sample consisted of 7012 participants (18 356 person-waves); mean (SD) age was 67.7 (10.0) years, 4131 (58.9%) were women, 1136 (16.2%) were non-Hispanic Black, 4849 (69.2%) were non-Hispanic White, and mean (SD) duration of schooling was 13.0 (3.0) years. Compared with food-secure older adults, experiencing low food security was associated with higher odds of dementia (odds ratio, 1.38; 95% CI, 1.15-1.67) as was experiencing very low food security (odds ratio, 1.37; 95% CI, 1.11-1.59). Low and very low food security was also associated with lower memory levels and faster age-related memory decline.
CONCLUSIONS AND RELEVANCE
In this cohort study of older US residents, food insecurity was associated with increased dementia risk, poorer memory function, and faster memory decline. Future studies are needed to examine whether addressing food insecurity may benefit brain health.
Topics: United States; Humans; Female; Middle Aged; Aged; Male; Alzheimer Disease; Cohort Studies; Agriculture; Algorithms; Memory Disorders
PubMed: 37988079
DOI: 10.1001/jamanetworkopen.2023.44186 -
Acta Neurochirurgica Oct 2023Since the late 1930s, electric brain stimulation (EBS) in awake patients has been known to occasionally elicit patient descriptions of a form of memory flashbacks, known... (Review)
Review
BACKGROUND
Since the late 1930s, electric brain stimulation (EBS) in awake patients has been known to occasionally elicit patient descriptions of a form of memory flashbacks, known as experiential phenomena. One understanding of these sensations are as caused by an augmentation of the capacity for memory retrieval. However, an alternative hypothesis holds that memory flashbacks during EBS are "synthetic constructions" in the form of mental events, falsely interpreted as memories.
METHODS
A critical narrative review is used to discuss the false memory hypothesis in relation to the current empirical literature and source attribution theory.
RESULTS
EBS as well as situational demands in the form of interaction between patient and neurosurgeon may both lead to the creation of mental events and influence their interpretation in a way that may create false memories. The false memory hypothesis provides a potential explanation for several apparent inconsistencies in the current literature such as (a) the fragmented nature of experiential reports, (b) the ability of EBS to induce memory retrieval errors in controlled studies, (c) that Penfield's elicitations of experiential phenomena are so rarely replicated in the modern era, and (d) the limited utility of techniques that elicit experiential phenomena in the treatment of memory disorders.
CONCLUSIONS
The hypothesis that experiential phenomena may largely be "synthetic constructions" deserves serious consideration by neurosurgeons.
Topics: Humans; Memory; Brain; Stereotaxic Techniques; Wakefulness; Electric Stimulation
PubMed: 35804269
DOI: 10.1007/s00701-022-05307-6 -
Biological Psychiatry Jun 2024Stressful events are ubiquitous in everyday life. The exposure to these stressors initiates the temporally orchestrated release of a multitude of hormones, peptides, and... (Review)
Review
Stressful events are ubiquitous in everyday life. The exposure to these stressors initiates the temporally orchestrated release of a multitude of hormones, peptides, and neurotransmitters that target brain areas critically implicated in learning and memory. This review summarizes recent insights on the profound impact of stress on four fundamental processes of memory: memory formation, memory contextualization, memory retrieval, and memory flexibility. Stress mediators instigate dynamic alterations in these processes, facilitating efficient responding under stress and the creation of a decontextualized memory representation that can effectively aid coping with novel future threats. While being generally adaptive, the same stress-related changes may contribute to rigid behaviors, uncontrollable intrusions, or generalized fear responding seen in anxiety disorders or posttraumatic stress disorder (PTSD). Drawing on recent discoveries in cognitive neuroscience and psychiatry, this review discusses how stress-induced alterations in memory processes can simultaneously foster adaptation to stressors and fuel psychopathology. The transition from adaptive to maladaptive changes in the impact of stress on memory hinges on the nuanced interplay of stressor characteristics and individual predispositions. Thus, taking individual differences in the cognitive response to stressors into account is essential for any successful treatment of stress-related mental disorders.
PubMed: 38880463
DOI: 10.1016/j.biopsych.2024.06.005 -
The New England Journal of Medicine Feb 2024
Topics: Humans; COVID-19; Memory, Episodic; Memory Disorders; Health Status; Prospective Studies
PubMed: 38416436
DOI: 10.1056/NEJMc2311200 -
Alzheimer's & Dementia : the Journal of... Feb 2024Although large-scale genome-wide association studies (GWAS) have been conducted on AD, few have been conducted on continuous measures of memory performance and memory...
INTRODUCTION
Although large-scale genome-wide association studies (GWAS) have been conducted on AD, few have been conducted on continuous measures of memory performance and memory decline.
METHODS
We conducted a cross-ancestry GWAS on memory performance (in 27,633 participants) and memory decline (in 22,365 participants; 129,201 observations) by leveraging harmonized cognitive data from four aging cohorts.
RESULTS
We found high heritability for two ancestry backgrounds. Further, we found a novel ancestry locus for memory decline on chromosome 4 (rs6848524) and three loci in the non-Hispanic Black ancestry group for memory performance on chromosomes 2 (rs111471504), 7 (rs4142249), and 15 (rs74381744). In our gene-level analysis, we found novel genes for memory decline on chromosomes 1 (SLC25A44), 11 (BSX), and 15 (DPP8). Memory performance and memory decline shared genetic architecture with AD-related traits, neuropsychiatric traits, and autoimmune traits.
DISCUSSION
We discovered several novel loci, genes, and genetic correlations associated with late-life memory performance and decline.
HIGHLIGHTS
Late-life memory has high heritability that is similar across ancestries. We discovered four novel variants associated with late-life memory. We identified four novel genes associated with late-life memory. Late-life memory shares genetic architecture with psychiatric/autoimmune traits.
Topics: Humans; Alzheimer Disease; Genome-Wide Association Study; Endophenotypes; Genetic Predisposition to Disease; Cognition; Memory Disorders; Polymorphism, Single Nucleotide
PubMed: 37985223
DOI: 10.1002/alz.13508 -
Dialogues in Clinical Neuroscience Dec 2023Craving, involving intense and urgent desires to engage in specific behaviours, is a feature of addictions. Multiple studies implicate regions of salience/limbic...
INTRODUCTION
Craving, involving intense and urgent desires to engage in specific behaviours, is a feature of addictions. Multiple studies implicate regions of salience/limbic networks and basal ganglia, fronto-parietal, medial frontal regions in craving in addictions. However, prior studies have not identified common neural networks that reliably predict craving across substance and behavioural addictions.
METHODS
Functional magnetic resonance imaging during an audiovisual cue-reactivity task and connectome-based predictive modelling (CPM), a data-driven method for generating brain-behavioural models, were used to study individuals with cocaine-use disorder and gambling disorder. Functions of nodes and networks relevant to craving were identified and interpreted based on meta-analytic data.
RESULTS
Craving was predicted by neural connectivity across disorders. The highest degree nodes were mostly located in the prefrontal cortex. Overall, the prediction model included complex networks including motor/sensory, fronto-parietal, and default-mode networks. The decoding revealed high functional associations with components of memory, valence ratings, physiological responses, and finger movement/motor imagery.
CONCLUSIONS
Craving could be predicted across substance and behavioural addictions. The model may reflect general neural mechanisms of craving despite specificities of individual disorders. Prefrontal regions associated with working memory and autobiographical memory seem important in predicting craving. For further validation, the model should be tested in diverse samples and contexts.
Topics: Humans; Craving; Gambling; Connectome; Substance-Related Disorders; Magnetic Resonance Imaging; Cocaine; Brain
PubMed: 37190759
DOI: 10.1080/19585969.2023.2208586 -
Genes Nov 2023Trauma in childhood and adolescence has long-term negative consequences in brain development and behavior and increases the risk for psychiatric disorders. Among them,... (Review)
Review
Trauma in childhood and adolescence has long-term negative consequences in brain development and behavior and increases the risk for psychiatric disorders. Among them, post-traumatic stress disorder (PTSD) during adolescence illustrates the connection between trauma and substance misuse, as adolescents may utilize substances to cope with PTSD. Drug misuse may in turn lead to neuroadaptations in learning processes that facilitate the consolidation of traumatic memories that perpetuate PTSD. This reflects, apart from common genetic and epigenetic modifications, overlapping neurocircuitry engagement triggered by stress and drug misuse that includes structural and functional changes in limbic brain regions and the salience, default-mode, and frontoparietal networks. Effective strategies to prevent PTSD are needed to limit the negative consequences associated with the later development of a substance use disorder (SUD). In this review, we will examine the link between PTSD and SUDs, along with the resulting effects on memory, focusing on the connection between the development of an SUD in individuals who struggled with PTSD in adolescence. Neuroimaging has emerged as a powerful tool to provide insight into the brain mechanisms underlying the connection of PTSD in adolescence and the development of SUDs.
Topics: Humans; Adolescent; Stress Disorders, Post-Traumatic; Substance-Related Disorders; Brain; Neuroimaging; Drug Misuse
PubMed: 38136935
DOI: 10.3390/genes14122113 -
Biomedicine & Pharmacotherapy =... Dec 2023Brain glucose hypometabolism is a significant manifestation of Alzheimer's disease (AD). 27-hydroxycholesterol (27-OHC) and the gut microbiota have been recognized as...
Brain glucose hypometabolism is a significant manifestation of Alzheimer's disease (AD). 27-hydroxycholesterol (27-OHC) and the gut microbiota have been recognized as factors possibly influencing the pathogenesis of AD. This study aimed to investigate the link between 27-OHC, the gut microbiota, and brain glucose uptake in AD. Here, 6-month-old male C57BL/6 J mice were treated with sterile water or antibiotic cocktails, with or without 27-OHC and/or 27-OHC synthetic enzyme CYP27A1 inhibitor anastrozole (ANS). The gut microbiota, brain glucose uptake levels, and memory ability were measured. We observed that 27-OHC altered microbiota composition, damaged brain tissue structures, decreased the 2-deoxy-2-[ F] fluorodeoxyglucose (F-FDG) uptake value, downregulated the gene expression of glucose transporter type 4 (GLUT4), reduced the colocalization of GLUT1/glial fibrillary acidic protein (GFAP) in the hippocampus, and impaired spatial memory. ANS reversed the effects of 27-OHC. The antibiotic-treated mice did not exhibit similar results after 27-OHC treatment. This study reveals a potential molecular mechanism wherein 27-OHC-induced memory impairment might be linked to reduced brain glucose uptake, mediated by the gut microbiota.
Topics: Mice; Male; Animals; Gastrointestinal Microbiome; Mice, Inbred C57BL; Brain; Alzheimer Disease; Memory Disorders; Glucose; Anti-Bacterial Agents
PubMed: 37806088
DOI: 10.1016/j.biopha.2023.115649 -
Cureus Oct 2023Connective tissue disorders (CTD) are a group of disorders affecting the connective tissues. Usually the musculoskeletal and the vascular system is impacted. Along with... (Review)
Review
Connective tissue disorders (CTD) are a group of disorders affecting the connective tissues. Usually the musculoskeletal and the vascular system is impacted. Along with these systems, the nervous system is also involved in CTD, which leads to various neurological manifestations. The pathophysiology of neurological complications of CTD is caused by various factors and is complicated. Disturbed immune complexes, chronic inflammation, and autoimmunity in which the body attacks its cells are considered to be responsible for the neurological complications of CTD. Additionally, the vascular symptoms that lead to decreased blood flow to the brain are also responsible for the neurological manifestations of CTD in diseases like systemic lupus erythematosus (SLE). In SLE, vessel wall integrity is compromised, which may lead to decreased blood flow leading to neurological complications. CTD can manifest a variety of neurological complications. These neurological complications can be classified into symptoms affecting the peripheral nervous system, central nervous system, and the autonomic nervous system. Some of the common neurological complications of CTD are headaches, seizures, ataxia, neuropathies leading to cranial nerve palsies, myelopathies, tremors, encephalitis, and cerebral infarction. Cranial nerve palsies can disturb sensations, vision, hearing, and mastication. Neuropsychiatric symptoms are also commonly observed in CTD. Cognitive dysfunction can be caused due to neuropsychiatric problems. Some of the cognitive dysfunctions are lack of concentration, memory loss, confusion, and coma. In this review, we will address various neurological manifestations of CTD.
PubMed: 38022020
DOI: 10.7759/cureus.47108 -
Translational Neurodegeneration Jan 2024Ageing is a crucial risk factor for Alzheimer's disease (AD) and is characterised by systemic changes in both intracellular and extracellular microenvironments that... (Review)
Review
Ageing is a crucial risk factor for Alzheimer's disease (AD) and is characterised by systemic changes in both intracellular and extracellular microenvironments that affect the entire body instead of a single organ. Understanding the specific mechanisms underlying the role of ageing in disease development can facilitate the treatment of ageing-related diseases, such as AD. Signs of brain ageing have been observed in both AD patients and animal models. Alleviating the pathological changes caused by brain ageing can dramatically ameliorate the amyloid beta- and tau-induced neuropathological and memory impairments, indicating that ageing plays a crucial role in the pathophysiological process of AD. In this review, we summarize the impact of several age-related factors on AD and propose that preventing pathological changes caused by brain ageing is a promising strategy for improving cognitive health.
Topics: Animals; Humans; Alzheimer Disease; Amyloid beta-Peptides; Aging; Brain; Memory Disorders
PubMed: 38254235
DOI: 10.1186/s40035-024-00397-x