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The International Journal of... Jun 2022Learning and memory functions in animals were evaluated by using Novel object recognition (NOR) and Morris water maze (MWM) tests. Following 7 days of LPS...
MATERIALS AND METHODS
Learning and memory functions in animals were evaluated by using Novel object recognition (NOR) and Morris water maze (MWM) tests. Following 7 days of LPS administration, animals were subjected to NOR test on Day-8 and MWM test on Days-9 to 13 for the assessment of recognition and spatial learning and memory, respectively.
RESULTS
LPS administration produced significant deficits in recognition and spatial memory in mice after seven days of LPS administration. In LPS pre-treated mice, agmatine treatment on Day-8 resulted in the increased exploration to the novel object. Agmatine treatment (Day 8-12) in mice showed reduction in the escape latency and time spent in the target quadrant (probe trial) in the MWM test. However, co-administration of agmatine with LPS in mice for 7 days showed higher discrimination index in NOR test on Day-8. This co-administration also decreased escape latency and time spent in the target quadrant in MWM test on Days 9-13 as compared to LPS control group.
CONCLUSION
Results implies the protective and curative effects of agmatine against LPS-induced loss of memory functions in experimental animals.HighlightsSubchronic but not acute lipopolysaccharides induce memory deficitsLipopolysaccharides impairs recognition and spatial memory in mice.Agmatine prevents lipopolysaccharides-induced loss of memory.Agmatine reverses deficits in learning and memory by lipopolysaccharides.
Topics: Agmatine; Animals; Hippocampus; Lipopolysaccharides; Maze Learning; Memory; Memory Disorders; Mice
PubMed: 33089716
DOI: 10.1080/00207454.2020.1830086 -
The Clinical Neuropsychologist Feb 2023To determine the longitudinal trajectories and normative standards of episodic memory in older adults.
OBJECTIVE
To determine the longitudinal trajectories and normative standards of episodic memory in older adults.
METHODS
Participants were drawn from the cognitively normal(CN) subgroup of the population-based HELIAD cohort, a fairly representative cohort of the older Greek population. Verbal and non-verbal memory were assessed using the Greek Verbal Learning Test and Medical College of Georgia-Complex Figure Test. Baseline and longitudinal associations of memory performance with age, sex and formal education were explored with linear regression analysis and generalized estimated equations.
RESULTS
A total of 1607 predominantly female (60%) individuals (73.82 ± 5.43 years), with a mean educational attainment of 8.17(±4.86) years were CN at baseline. Baseline analysis revealed a continuum of memory decline with aging and lower educational attainment. Women performed better in composite and verbal memory measures, while men performed better in non-verbal memory tasks. A subgroup of 761 participants with available assessments after 3.07(±0.82) years remained CN at follow-up. Composite memory scores yearly diminished by an additional 0.007 of a SD for each additional year of age at baseline. Regarding verbal learning, immediate free verbal recall, delayed free verbal recall and delayed cued verbal recall, an additional yearly decrease of 0.107, 0.043, 0.036 and 0.026 words were respectively recorded at follow-up, for each additional year of age at baseline. Women underwent steeper yearly decreases of 0.227 words in delayed cued verbal recall. No significant longitudinal associations emerged for immediate non-verbal memory, delayed non-verbal memory and immediate cued verbal recall.
CONCLUSIONS
In the present study, aging (but not educational attainment) was consistently associated with steeper verbal memory decline.
UNLABELLED
Supplemental data for this article is available online at https://doi.org/10.1080/13854046.2022.2059011 .
Topics: Male; Humans; Female; Aged; Memory, Episodic; Neuropsychological Tests; Aging; Cognition; Memory Disorders; Longitudinal Studies
PubMed: 35400289
DOI: 10.1080/13854046.2022.2059011 -
Journal of Clinical and Experimental... Apr 2022The present study aims to examine whether declarative memory dysfunction relates to impaired core memory mechanisms or attentional and executive dysfunction in... (Observational Study)
Observational Study
OBJECTIVE
The present study aims to examine whether declarative memory dysfunction relates to impaired core memory mechanisms or attentional and executive dysfunction in idiopathic REM Sleep Behavior Disorder (iRBD).
METHOD
In this observational, cross-sectional study, were enrolled 82 individuals with the diagnosis of iRBD according to the International Classification of Sleep Disorders and 49-matched healthy controls fulfilling inclusion criteria. All participants underwent two memory tasks, namely the Rey Auditory Verbal Learning Test (RAVLT) and Memory Binding Test (MBT), which include conditions of varying degrees of dependence on executive functioning, as well as different indicators of core memory processes (e.g., learning, retention, relational binding).
RESULTS
We used Bayesian multivariate generalized linear model analysis to evaluate the effect of iRBD on memory performance controlled for effects of age and sex. Individuals with iRBD displayed worse memory performance in the delayed free recall task ( = -0.37, 95% PPI [-0.69, -0.05]), but not on delayed recognition of the same material. Their performance in cued recall tasks both in immediate and delayed conditions was in comparison to controls relatively spared. Moreover, the deficit in delayed free recall was mediated by attention/processing speed.
CONCLUSIONS
In iRBD, we replicated findings of reduced free recall based on inefficient retrieval (retrieval deficit), which was small in terms of effect size. Importantly, the memory profile across measures does not support the presence of core memory dysfunction, such as poor learning, retention or associative binding.
Topics: Bayes Theorem; Cognitive Dysfunction; Cross-Sectional Studies; Humans; Memory Disorders; Neuropsychological Tests; REM Sleep Behavior Disorder
PubMed: 35986521
DOI: 10.1080/13803395.2022.2107182 -
Journal of Neurodevelopmental Disorders Nov 2023ATRX is an ATP-dependent chromatin remodeling protein with essential roles in safeguarding genome integrity and modulating gene expression. Deficiencies in this protein...
BACKGROUND
ATRX is an ATP-dependent chromatin remodeling protein with essential roles in safeguarding genome integrity and modulating gene expression. Deficiencies in this protein cause ATR-X syndrome, a condition characterized by intellectual disability and an array of developmental abnormalities, including features of autism. Previous studies demonstrated that deleting ATRX in mouse forebrain excitatory neurons postnatally resulted in male-specific memory deficits, but no apparent autistic-like behaviours.
METHODS
We generated mice with an earlier embryonic deletion of ATRX in forebrain excitatory neurons and characterized their behaviour using a series of memory and autistic-related paradigms.
RESULTS
We found that mutant mice displayed a broader spectrum of impairments, including fear memory, decreased anxiety-like behaviour, hyperactivity, as well as self-injurious and repetitive grooming. Sex-specific alterations were also observed, including male-specific aggression, sensory gating impairments, and decreased social memory.
CONCLUSIONS
Collectively, the findings indicate that early developmental abnormalities arising from ATRX deficiency in forebrain excitatory neurons contribute to the presentation of fear memory deficits as well as autistic-like behaviours.
Topics: Female; Mice; Male; Animals; Autistic Disorder; Neurons; Memory Disorders; Cognition
PubMed: 37957569
DOI: 10.1186/s11689-023-09508-7 -
International Journal of Molecular... Mar 2021Sulforaphane, a potent dietary bioactive agent obtainable from cruciferous vegetables, has been extensively studied for its effects in disease prevention and therapy.... (Review)
Review
Sulforaphane, a potent dietary bioactive agent obtainable from cruciferous vegetables, has been extensively studied for its effects in disease prevention and therapy. Sulforaphane potently induces transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated expression of detoxification, anti-oxidation, and immune system-modulating enzymes, and possibly acts as an anti-carcinogenic agent. Several clinical trials are in progress to study the effect of diverse types of cruciferous vegetables and sulforaphane on prostate cancer, breast cancer, lung cancer, atopic asthmatics, skin aging, dermatitis, obesity, etc. Recently, the protective effects of sulforaphane on brain health were also considerably studied, where the studies have further extended to several neurological diseases, including Alzheimer's disease (AD), Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, autism spectrum disorder, and schizophrenia. Animal and cell studies that employ sulforaphane against memory impairment and AD-related pre-clinical biomarkers on amyloid-β, tau, inflammation, oxidative stress, and neurodegeneration are summarized, and plausible neuroprotective mechanisms of sulforaphane to help prevent AD are discussed. The increase in pre-clinical evidences consistently suggests that sulforaphane has a multi-faceted neuroprotective effect on AD pathophysiology. The anti-AD-like evidence of sulforaphane seen in cells and animals indicates the need to pursue sulforaphane research for relevant biomarkers in AD pre-symptomatic populations.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Biomarkers; Cell Line, Tumor; Disease Models, Animal; Drug Administration Schedule; Drug Evaluation, Preclinical; Gene Expression Regulation; Humans; Isothiocyanates; Memory Disorders; Neurons; Neuroprotective Agents; Oxidative Stress; Protein Aggregates; Sulfoxides; tau Proteins
PubMed: 33805772
DOI: 10.3390/ijms22062929 -
Oxidative Medicine and Cellular... 2020This study was conducted to assess the protective effect of extract of match (EM) on high-fat diet- (HFD-) induced cognitive deficits in male C57BL/6 mice. It was found...
This study was conducted to assess the protective effect of extract of match (EM) on high-fat diet- (HFD-) induced cognitive deficits in male C57BL/6 mice. It was found that EM improved glucose tolerance status by measuring OGTT and IPGTT with HFD-induced mice. EM protected behavioral and memory dysfunction in Y-maze, passive avoidance, and Morris water maze tests. Consumption of EM reduced fat mass, dyslipidemia, and inflammation in adipose tissue. Also, EM ameliorated hepatic and cerebral antioxidant systems. EM improved the cerebral cholinergic system by regulating ACh contents and expression of AChE and ChAT. Also, EM restored mitochondrial function in liver and brain tissue. EM attenuated hepatic inflammatory effect, lipid synthesis, and cholesterol metabolism by regulating the protein expression of TNF-, TNFR1, -IRS-1, -JNK, IL-1, iNOS, COX-2, HMGCR, PPAR, and FAS. Finally, EM regulated cognitive function and neuroinflammation in the whole brain, hippocampus, and cerebral cortex by regulating the protein expression of -JNK, -Akt, -tau, A, BDNF, IDE, COX-2, and IL-1. These findings suggest that EM might be a potential source of functional food to improve metabolic disorder-associated cognitive dysfunction.
Topics: Adipose Tissue; Animals; Cognitive Dysfunction; Diet, High-Fat; Dyslipidemias; Gene Expression Regulation; Inflammation; Male; Memory Disorders; Mice; Panniculitis; Tea
PubMed: 33312340
DOI: 10.1155/2020/8882763 -
Journal of Clinical and Experimental... Feb 2022Persistent memory complaints following concussion often do not coincide with evidence of objective memory impairment. To the extent this clinical presentation represents...
INTRODUCTION
Persistent memory complaints following concussion often do not coincide with evidence of objective memory impairment. To the extent this clinical presentation represents Functional Cognitive Disorder (FCD), we would expect preservation or even enhancement of memory for instances of forgetting, based on two lines of prior evidence. First, emotional arousal enhances autobiographical memory. People who experience memory lapses as worrisome may better remember them. Second, individuals with FCD can paradoxically provide detailed accounts of memory lapses compared to patients with neurodegenerative disease, who tend to provide vague examples. The current study aimed to better characterize the recall of forgetting events in people with subjective memory problems following concussion.
METHODS
The study sample consisted of adults with chronic post-concussion symptoms (N = 37, M = 42.7 years old; 70.27% women; M = 24.9 months post-injury) and normal-range performance on conventional neuropsychological tests. Participants completed a measure of memory complaint severity and the Autobiographical Interview (AI). The AI was used to quantify the richness of narrative recollections of recent instances when they forgot something and (control) personal events that did not involve forgetting. Linear regression modeling assessed the relationship between memory complaint severity and AI variables, including narrative details, valence, arousal, and rehearsal of memories.
RESULTS
There was no association between memory complaint severity and memory for forgetting vs. control events. We further found no association between memory complaint severity and AI performance overall (collapsing across forgetting and control events). Participants with greater memory complaints experienced past memory lapses as more negative than control memories, but did not consistently differ on other AI phenomenological variables.
CONCLUSION
Autobiographical recall of memory lapses appears preserved but not selectively heightened in people who report experiencing severe memory problems long after concussion. This inconsistency supports conceptualization of persistent memory complaints after concussion as FCD.
Topics: Adult; Brain Concussion; Female; Humans; Male; Memory Disorders; Memory, Episodic; Mental Recall; Neurodegenerative Diseases; Neuropsychological Tests; Post-Concussion Syndrome
PubMed: 35536243
DOI: 10.1080/13803395.2022.2067326 -
Pharmacological Research Jan 2021Gintonin is a novel glycolipoprotein, which has been abundantly found in the root of Korean ginseng. It holds lysophosphatidic acids (LPAs), primarily identified LPA... (Review)
Review
Gintonin is a novel glycolipoprotein, which has been abundantly found in the root of Korean ginseng. It holds lysophosphatidic acids (LPAs), primarily identified LPA C18:2, and is an exogenous agonist of LPA receptors (LPARs). Gintonin maintains blood-brain barrier integrity, and it has recently been studied in several models of neurodegenerative diseases (NDDs) such as Alzheimer's disease (AD), Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis. Gintonin demonstrated neuroprotective activity by providing action against neuroinflammation-, apoptosis- and oxidative stress-mediated neurodegeneration. Gintonin showed an emerging role as a modulator of synaptic transmission and neurogenesis and also potentially regulated autophagy in primary cortical astrocytes. It also ameliorated the toxic agent-induced and genetic models of cognitive deficits in experimental NDDs. As a novel agonist of LPARs, gintonin regulated several G protein-coupled receptors (GPCRs) including GPR40 and GPR55. However, further study needs to be investigated to understand the underlying mechanism of action of gintonin in memory disorders.
Topics: Animals; Humans; Memory Disorders; Neuroprotective Agents; Plant Extracts
PubMed: 33007419
DOI: 10.1016/j.phrs.2020.105221 -
Environmental Science and Pollution... Jan 2023Learning and memory play a fundamental role on brain cognitive functions which are crucial for human life. Nonylphenol (NP), a serious environmental pollutant over the... (Review)
Review
Learning and memory play a fundamental role on brain cognitive functions which are crucial for human life. Nonylphenol (NP), a serious environmental pollutant over the world, is proven to be harmful for learning and memory mainly via diet exposure. Currently, besides the administrative restrictions for the use of NP, there are rarely other effective approaches against learning and memory impairment caused by NP. This review summarized the mechanisms underlying NP-induced learning and memory impairment according to in vivo and in vitro experiments. Based on the studies involved in behavior tests, these mechanisms were classified as oxidative stress, neurotransmitter disorder, synaptic plasticity impairment, and neuron injury. In addition, according to the studies which did not conduct behavior tests, the possible mechanisms underlying NP-induced learning and memory impairment were proposed as chronic inflammation and gut permeability increment. Furthermore, this review also revealed the demanding questions for the mechanism investigations and therapeutic methods. Notably, the summarized mechanisms might accelerate the prevention and remediation of NP-induced learning and memory impairment.
Topics: Humans; Learning; Memory Disorders; Brain; Phenols; Hippocampus
PubMed: 36434456
DOI: 10.1007/s11356-022-24278-w -
Neuropsychology Sep 2022Memory deficits in individuals with schizophrenia are well-established, but less is known about how schizophrenia affects metacognitive processes such as metamemory. We...
OBJECTIVE
Memory deficits in individuals with schizophrenia are well-established, but less is known about how schizophrenia affects metacognitive processes such as metamemory. We investigated metamemory ability using the value-directed remembering task, which assesses the degree to which participants use value cues to guide their learning of a list of items (i.e., their memory selectivity).
METHOD
Participants were patients undergoing treatment following a recent first episode of schizophrenia ( = 20) and demographically comparable healthy controls ( = 18). Participants viewed six lists of 24 words where each word was paired with either a low value (1-3 points) or a high value (10-12 points), and they were instructed to maximize their score on free recall tests given after each list. After the final free recall test, participants completed a recognition test where they gave remember/know judgments.
RESULTS
On tests of free recall, patients showed reduced memory selectivity relative to healthy controls. On the recognition test, patients failed to show an effect of value on recognition of nonrecalled words, in contrast to healthy controls, who showed a significant value effect that was characterized by greater "remember" judgments. Patients initially overestimated their memory capacity but were able to adjust their estimates to be more accurate based on task experience. Patients' self-reports of memory selectivity were unrelated to their actual memory selectivity.
CONCLUSIONS
Patients with first-episode schizophrenia had substantial impairments on the value-directed remembering task, but areas of preserved metamemory ability were also observed. These findings have potential implications for cognitive training interventions. (PsycInfo Database Record (c) 2022 APA, all rights reserved).
Topics: Humans; Memory Disorders; Mental Recall; Metacognition; Recognition, Psychology; Schizophrenia
PubMed: 35737534
DOI: 10.1037/neu0000840