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Neuroscience and Biobehavioral Reviews Jan 2020The purpose of this review is to illustrate how a reductionistic, but sophisticated, approach based on the use of a simple model system such as the pond snail Lymnaea... (Review)
Review
The purpose of this review is to illustrate how a reductionistic, but sophisticated, approach based on the use of a simple model system such as the pond snail Lymnaea stagnalis (L. stagnalis), might be useful to address fundamental questions in learning and memory. L. stagnalis, as a model, provides an interesting platform to investigate the dialog between the synapse and the nucleus and vice versa during memory and learning. More importantly, the "molecular actors" of the memory dialogue are well-conserved both across phylogenetic groups and learning paradigms, involving single- or multi-trials, aversion or reward, operant or classical conditioning. At the same time, this model could help to study how, where and when the memory dialog is impaired in stressful conditions and during aging and neurodegeneration in humans and thus offers new insights and targets in order to develop innovative therapies and technology for the treatment of a range of neurological and neurodegenerative disorders.
Topics: Aging; Animals; Lymnaea; Memory; Memory Disorders; Models, Animal; Neurosciences; Stress, Psychological; Translational Research, Biomedical
PubMed: 31786320
DOI: 10.1016/j.neubiorev.2019.11.020 -
Trends in Psychiatry and Psychotherapy Jun 2020Introduction Children with anxiety disorders have been suggested to possess deficits in verbal fluency, shifting and attention, with inconsistent results regarding...
Introduction Children with anxiety disorders have been suggested to possess deficits in verbal fluency, shifting and attention, with inconsistent results regarding working memory and its subcomponents. This study extends previous findings by analyzing the performance of children with anxiety disorders in a wide range of neuropsychological functions. Methods We evaluated 54 children with a primary diagnosis of an anxiety disorder according to diagnostic criteria from the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) using subtests of a neuropsychological battery. The severity of anxiety disorders was assessed using the Pediatric Anxiety Rating Scale (PARS). We calculated the frequency of neuropsychological impairments (-1.5 standard deviation of the normative sample). Comparisons between groups were performed based on the severity of anxiety symptoms, as well as in the presence of one vs. more diagnoses of anxiety disorder. Results We found higher impairment in visuospatial working memory (23.1%), semantic memory (27.8%), oral language (35.4%) and word writing (44.4%) in anxious children. Moreover, children with higher anxiety severity presented lower performance in visuospatial working memory, inferential processing, word reading, writing comprehension, copied writing, and semantic verbal fluency (d = 0.49 to 0.96 [Cohen's d]). The higher the number of anxiety diagnoses, the lower the performance in episodic memory and oral and written language (d = 0.56 to 0.77). Conclusion Our data suggested the presence of memory (visuospatial working memory and semantic memory) and language deficits (oral and writing) in some children with an anxiety disorder. Severity and number of anxiety diagnoses were associated with lower performance in memory and language domains in childhood.
Topics: Anxiety Disorders; Anxiety, Separation; Child; Cognitive Dysfunction; Female; Humans; Language Disorders; Male; Memory Disorders; Phobia, Social; Severity of Illness Index
PubMed: 32696887
DOI: 10.1590/2237-6089-2019-0051 -
FASEB Journal : Official Publication of... Nov 2019Memory deficits affect a large proportion of the human population and are associated with aging and many neurologic, neurodegenerative, and psychiatric diseases....
Memory deficits affect a large proportion of the human population and are associated with aging and many neurologic, neurodegenerative, and psychiatric diseases. Treatment of this mental disorder has been disappointing because all potential candidates studied thus far have failed to produce consistent effects across various types of memory and have shown limited to no effects on memory deficits. Here, we show that the promotion of neuronal arborization through the expression of the regulator of G-protein signaling 14 of 414 amino acids (RGS14) not only induced robust enhancement of multiple types of memory but was also sufficient for the recovery of recognition, spatial, and temporal memory, which are kinds of episodic memory that are primarily affected in patients or individuals with memory dysfunction. We observed that a surge in neuronal arborization was mediated by up-regulation of brain-derived neurotrophic factor (BDNF) signaling and that the deletion of BDNF abrogated both neuronal arborization activation and memory enhancement. The activation of BDNF-dependent neuronal arborization generated almost 2-fold increases in synapse numbers in dendrites of pyramidal neurons and in neurites of nonpyramidal neurons. This increase in synaptic connections might have evoked reorganization within neuronal circuits and eventually supported an increase in the activity of such circuits. Thus, in addition to showing the potential of RGS14 for rescuing memory deficits, our results suggest that a boost in circuit activity could facilitate memory enhancement and the reversal of memory deficits.-Masmudi-Martín, M., Navarro-Lobato, I., López-Aranda, M. F., Delgado, G., Martín-Montañez, E., Quiros-Ortega, M. E., Carretero-Rey, M., Narváez, L., Garcia-Garrido, M. F., Posadas, S., López-Téllez, J. F., Blanco, E., Jiménez-Recuerda, I., Granados-Durán, P., Paez-Rueda, J., López, J. C., Khan, Z. U. RGS14 treatment induces memory enhancement and rescues episodic memory deficits.
Topics: Animals; Brain; Hippocampus; Memory Disorders; Memory, Episodic; Mice; Neurites; Neuronal Plasticity; Neurons; Peptide Fragments; RGS Proteins; Rats; Signal Transduction; Synapses
PubMed: 31365833
DOI: 10.1096/fj.201900429RR -
BMC Psychiatry Aug 2022Visual memory impairment is one of the most commonly complained symptoms in patients with major depressive disorder (MDD). Pattern glare is also a distorted visual...
BACKGROUND
Visual memory impairment is one of the most commonly complained symptoms in patients with major depressive disorder (MDD). Pattern glare is also a distorted visual phenomenon that puzzles patients with MDD. Nevertheless, how these two phenomena interact in MDD remains unknown. This study investigated the association between pattern glare and visual memory in MDD patients.
METHODS
Sixty-two patients with MDD and forty-nine age-, sex- and education level-matched healthy controls (HCs) were included in this study. The Pattern Recognition Memory (PRM) test and the Brief Visual Memory Test-Revised (BVMT-R) were applied to measure visual memory. The pattern glare test including three patterns with different spatial frequencies (SFs) was used to explore pattern glare levels.
RESULTS
Patients with MDD scored lower on the PRM-PCi, BVMT-R1, BVMT-R2, BVMT-R3, and BVMT-Rt and higher on the PRM-MCLd than HCs (all p < 0.05). Pattern glare scores for MDD patients were higher with mid-SF (p < 0.001), high-SF (p = 0.006) and mid-high SF differences (p = 0.01) than for HCs. A positive correlation between mid-SF and PRM-MCLd scores in all participants was observed (p = 0.01, r = 0.246). A negative correlation between mid-high difference scores and BVMT-R2 scores (p = 0.032, r = -0.317) was observed in HCs, but no significant correlation was observed in MDD patients.
CONCLUSIONS
The present study showed that visual memory and pattern glare are disrupted in MDD. Visual memory may be associated with pattern glare and needs to be studied in future work.
Topics: Depressive Disorder, Major; Glare; Humans; Memory; Memory Disorders
PubMed: 35918667
DOI: 10.1186/s12888-022-04167-9 -
Journal of Acquired Immune Deficiency... Feb 2022Brain-derived neurotrophic factor (BDNF) shows consistent associations with memory across many clinical populations, including dementia. Less is understood about the...
BACKGROUND
Brain-derived neurotrophic factor (BDNF) shows consistent associations with memory across many clinical populations, including dementia. Less is understood about the association between BDNF and memory functioning in people living with HIV (PWH).
METHODS
A sample of 173 adults aged 50+ (n = 100 HIV+ and n = 73 HIV seronegative) completed a comprehensive neurobehavioral assessment and blood draw. Linear regressions predicting memory domains (learning, delayed recall, and recognition) were conducted including race (White vs. Black/African American), HIV status, BDNF, and their interactions.
RESULTS
For learning and delayed recall, significant (P < 0.05) main effects for race and interactions for BDNF x race and HIV status x race were found, whereas for recognition, only a BDNF x race interaction emerged. In adjusted models, BDNF x race interactions remained for learning and delayed recall. To determine effect size, correlations were conducted between BDNF and memory domains stratified by HIV serostatus and race, and small-medium associations between BDNF and learning and delayed recall (rho = 0.29, P < 0.01; rho = 0.22, P = 0.045), but no recognition (rho = 0.12, P = 0.29) were found among Black/African American PWH. BDNF was not significantly associated with memory domains in White PWH or either HIV- sample. Follow-up analyses showed BDNF-memory specificity, such that race X BDNF interactions did not emerge for other cognitive domains.
CONCLUSIONS
While limited by cross-sectional design among a small sample, particularly of White individuals, results indicate that BDNF may serve as a promising biomarker reflecting memory functioning in PWH, particularly Black/African Americans. Further work is needed to replicate findings and determine mechanisms for racial differences in BDNF associations with memory.
Topics: Adult; Black or African American; Black People; Brain-Derived Neurotrophic Factor; Cognition; Cross-Sectional Studies; HIV Infections; Humans; Memory; Memory Disorders; Middle Aged; White People
PubMed: 34629411
DOI: 10.1097/QAI.0000000000002831 -
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 -
International Journal of Molecular... Aug 2023Memories are a central aspect of our lives, but the mechanisms underlying their formation, consolidation, retrieval, and extinction remain poorly understood. In this... (Review)
Review
Memories are a central aspect of our lives, but the mechanisms underlying their formation, consolidation, retrieval, and extinction remain poorly understood. In this review, we explore the molecular mechanisms of memory modulation and investigate the effects of RNA on these processes. Specifically, we examine the effects of time and location on gene expression alterations. We then discuss the potential for harnessing these alterations to modulate memories, particularly fear memories, to alleviate post-traumatic stress disorder (PTSD) symptoms. The current state of research suggests that transcriptional changes play a major role in memory modulation and targeting them through microRNAs may hold promise as a novel approach for treating memory-related disorders such as PTSD.
Topics: Humans; Stress Disorders, Post-Traumatic; MicroRNAs; Fear; Memory Disorders
PubMed: 37629089
DOI: 10.3390/ijms241612908 -
Neuropsychology Sep 2020Attention-deficit/hyperactivity disorder (ADHD) has been associated with large magnitude impairments in working memory, whereas short-term memory deficits, when...
Attention-deficit/hyperactivity disorder (ADHD) has been associated with large magnitude impairments in working memory, whereas short-term memory deficits, when detected, tend to be less pronounced. However, confidence in these findings is limited due to task impurity combined with methodological and statistical limitations of the current evidence base. A well-characterized, clinically evaluated sample of 172 children ages 8-13 years ( = 10.30, = 1.42; 72 girls; 64% White/non-Hispanic) were administered multiple, counterbalanced working memory tests. Bifactor-(s-1) modeling was used to characterize the presence and magnitude of central executive working memory, phonological short-term memory, and visuospatial short-term memory deficits in pediatric ADHD. ADHD status was associated with very large magnitude impairments in central executive working memory that are present in most pediatric cases ( = 1.63-2.03; 75%-81% impaired), and these deficits covaried with ADHD inattentive and hyperactive/impulsive symptom severity based on both parent and teacher report. There was also evidence for a unique, albeit significantly smaller, impairment in visuospatial short-term memory ( = 0.60; 38% impaired); however, visuospatial short-term memory abilities did not covary with ADHD symptom severity. There was no evidence linking ADHD with phonological short-term memory deficits across either the dimensional or categorical analyses. These findings provide strong evidence that ADHD is associated with marked central executive working memory deficits that covary with their behavioral symptom presentation across settings. In contrast, visuospatial short-term memory deficits, when present, are likely epiphenomenal, and the most parsimonious conclusion appears to be that phonological short-term memory is intact in pediatric ADHD. (PsycInfo Database Record (c) 2020 APA, all rights reserved).
Topics: Adolescent; Attention Deficit Disorder with Hyperactivity; Child; Executive Function; Female; Humans; Male; Memory Disorders; Memory, Short-Term; Models, Psychological; Neuropsychological Tests; Parents; School Teachers; Spatial Memory
PubMed: 32437194
DOI: 10.1037/neu0000641 -
Frontiers in Endocrinology 2021Sleep is a critical biological process, essential for cognitive well-being. Neuroscientific literature suggests there are mechanistic relations between sleep disruption... (Review)
Review
Sleep is a critical biological process, essential for cognitive well-being. Neuroscientific literature suggests there are mechanistic relations between sleep disruption and memory deficits, and that varying concentrations of cortisol may play an important role in mediating those relations. Patients with Addison's disease (AD) experience consistent and predictable periods of sub- and supra-physiological cortisol concentrations due to lifelong glucocorticoid replacement therapy, and they frequently report disrupted sleep and impaired memory. These disruptions and impairments may be related to the failure of replacement regimens to restore a normal circadian rhythm of cortisol secretion. Available data provides support for existing theoretical frameworks which postulate that in AD and other neuroendocrine, neurological, or psychiatric disorders, disrupted sleep is an important biological mechanism that underlies, at least partially, the memory impairments that patients frequently report experiencing. Given the literature linking sleep disruption and cognitive impairment in AD, future initiatives should aim to improve patients' cognitive performance (and, indeed, their overall quality of life) by prioritizing and optimizing sleep. This review summarizes the literature on sleep and cognition in AD, and the role that cortisol concentrations play in the relationship between the two.
Topics: Addison Disease; Cognition; Humans; Hydrocortisone; Memory Disorders; Quality of Life; Risk Factors; Signal Transduction; Sleep
PubMed: 34512546
DOI: 10.3389/fendo.2021.694046 -
Neurobiology of Disease Jun 2023Epilepsy is a comorbidity associated with Alzheimer's disease (AD), often starting many years earlier than memory decline. Investigating this association in the early...
Epilepsy is a comorbidity associated with Alzheimer's disease (AD), often starting many years earlier than memory decline. Investigating this association in the early pre-symptomatic stages of AD can unveil new mechanisms of the pathology as well as guide the use of antiepileptic drugs to prevent or delay hyperexcitability-related pathological effects of AD. We investigated the impact of repeated seizures on hippocampal memory and amyloid-β (Aβ) load in pre-symptomatic Tg2576 mice, a transgenic model of AD. Seizure induction caused memory deficits and an increase in oligomeric Aβ and fibrillary species selectively in pre-symptomatic transgenic mice, and not in their wildtype littermates. Electrophysiological patch-clamp recordings in ex vivo CA1 pyramidal neurons and immunoblots were carried out to investigate the neuronal alterations associated with the behavioral outcomes of Tg2576 mice. CA1 pyramidal neurons exhibited increased intrinsic excitability and lower hyperpolarization-activated I current. CA1 also displayed lower expression of the hyperpolarization-activated cyclic nucleotide-gated HCN1 subunit, a protein already identified as downregulated in the AD human proteome. The antiepileptic drug lamotrigine restored electrophysiological alterations and prevented both memory deficits and the increase in extracellular Aβ induced by seizures. Thus our study provides evidence of pre-symptomatic hippocampal neuronal alterations leading to hyperexcitability and associated with both higher susceptibility to seizures and to AD-specific seizure-induced memory impairment. Our findings also provide a basis for the use of the antiepileptic drug lamotrigine as a way to counteract acceleration of AD induced by seizures in the early phases of the pathology.
Topics: Mice; Humans; Animals; Alzheimer Disease; Anticonvulsants; Lamotrigine; Hippocampus; Amyloid beta-Peptides; Seizures; Mice, Transgenic; Disease Models, Animal; Memory Disorders
PubMed: 37001613
DOI: 10.1016/j.nbd.2023.106106