Change Memory Research Articles

Chronic ultraviolet irradiation induces memory deficits via dysregulation of the dopamine pathway

The effects of ultraviolet (UV) radiation on brain function have previously been investigated; however, the specific neurotransmitter-mediated mechanisms responsible for UV radiation-induced neurobehavioral changes remain elusive. In this study, we aimed to explore the mechanisms underlying UV radiation-induced neurobehavioral changes. In a mouse model, we observed that UV irradiation of the skin induces deficits in hippocampal memory, synaptic plasticity, and adult neurogenesis, as well as increased dopamine levels in the skin, adrenal glands, and brain. Chronic UV exposure altered the expression of genes involved in dopaminergic neuron differentiation. Furthermore, chronic peripheral dopamine treatments resulted in memory deficits. Systemic administration of a dopamine D1/D5 receptor antagonist reversed changes in memory, synaptic plasticity, adult neurogenesis, and gene expression in UV-irradiated mice. Our findings provide converging evidence that chronic UV exposure alters dopamine levels in the central nervous system and peripheral organs, including the skin, which may underlie the observed neurobehavioral shifts, such as hippocampal memory deficits and impaired neurogenesis. This study underscores the importance of protection from UV exposure and introduces the potential of pharmacological approaches targeting dopamine receptors to counteract the adverse neurological impacts of UV exposure.

Chronic administration of caffeine, modafinil, AVL-3288 and CX516 induces time-dependent complex effects on cognition and mood in an animal model of sleep deprivation

ObjectiveCaffeine and modafinil are used to reverse effects of sleep deprivation. Nicotinic alpha-7 receptor and AMPA receptor positive allosteric modulators (PAM) are also potential substances in this context. Our objective is to evaluate the effects of caffeine, modafinil, AVL-3288 (nicotinic alpha-7 PAM) and CX516 (AMPA receptor PAM) on cognition and mood in a model of sleep deprivation. MethodModified multiple platform model is used to sleep-deprive mice for 24 days, for 8 h/day. Vehicle, Modafinil (40 mg/kg), Caffeine (5 mg/kg), CX516 (10 mg/kg), and AVL3288 (1 mg/kg) were administered intraperitoneally daily. A cognitive test battery was applied every six days for four times. The battery that included elevated plus maze, novel object recognition, and sucrose preference tests was administered on consecutive days. ResultsSleep deprivation decreased novel object recognition skill, but no significant difference was found in anxiety and depressive mood. Caffeine administration decreased anxiety-like behavior in short term, but this effect disappeared in chronic administration. Caffeine administration increased memory performance in chronic period. AVL group showed better memory performance in short term, but this effect disappeared in the rest of experiment. Although, in the modafinil group, no significant change in mood and memory was observed, anhedonia was observed in the chronic period in vehicle, caffeine and modafinil groups, but not in AVL-3288 and CX-516 groups. ConclusionCaffeine has anxiolytic effect in acute administration. The improvement of memory in chronic period may be associated with the neuroprotective effects of caffeine. AVL-3288 had a short-term positive effect on memory, but tolerance to these effects developed over time. Furthermore, no anhedonia was observed in AVL-3288 and CX516 groups in contrast to vehicle, caffeine and modafinil groups. This indicates that AVL-3288 and CX516 may show protective effect against depression.

Association of the oral microbiome with cognitive function among older adults: NHANES 2011–2012

BackgroundAn association between the gut microbiome and cognitive function has been demonstrated in prior studies. However, whether the oral microbiome, the second largest microbial habitant in humans, has a role in cognition remains unclear. Design, setting, participantsUsing weighted data from the 2011 to 2012 National Health and Nutrition Examination Survey, we examined the association between oral microbial composition and cognitive function in older adults. The oral microbiome was characterized by 16S ribosomal RNA gene sequencing. Cognitive status was assessed using the Consortium to Establish a Registry for Alzheimer’s Disease immediate recall and delayed recall, Animal Fluency Test, and Digit Symbol Substitution Test (DSST). Subjective memory changes over 12 months were also assessed. Linear and logistic regression models were conducted to quantify the association of α-diversity with different cognitive measurements controlling for potential confounding variables. Differences in β-diversity were analyzed using permutational analysis of variance. ResultsA total of 605 participants aged 60–69 years were included in the analysis. Oral microbial α-diversity was significantly and positively correlated with DSST (β, 2.92; 95% CI, 1.01–4.84). Participants with higher oral microbial α-diversity were more likely to have better cognitive performance status based on DSST (adjusted odds ratio, 2.35; 95% CI, 1.28–4.30) and were less likely to experience subjective memory changes (adjusted odds ratio, 0.43; 95% CI, 0.25–0.74). In addition, β-diversity was statistically significant for the cognitive performance status based on DSST (P = 0.031) and subjective memory changes (P = 0.023). ConclusionsOral microbial composition was associated with executive function and subjective memory changes among older adults among older U.S. adults in a nationally representative population sample. Oral dysbiosis is a potential biomarker or therapeutic target for cognitive decline. Further work is needed to elucidate the mechanisms underpinning the association between the oral microbiome and cognitive function.

Counterfactual thinking induces different neural patterns of memory modification in anxious individuals

Episodic counterfactual thinking (eCFT) is the process of mentally simulating alternate versions of experiences, which confers new phenomenological properties to the original memory and may be a useful therapeutic target for trait anxiety. However, it remains unclear how the neural representations of a memory change during eCFT. We hypothesized that eCFT-induced memory modification is associated with changes to the neural pattern of a memory primarily within the default mode network, moderated by dispositional anxiety levels. We tested this proposal by examining the representational dynamics of eCFT for 39 participants varying in trait anxiety. During eCFT, lateral parietal regions showed progressively more distinct activity patterns, whereas medial frontal neural activity patterns became more similar to those of the original memory. Neural pattern similarity in many default mode network regions was moderated by trait anxiety, where highly anxious individuals exhibited more generalized representations for upward eCFT (better counterfactual outcomes), but more distinct representations for downward eCFT (worse counterfactual outcomes). Our findings illustrate the efficacy of examining eCFT-based memory modification via neural pattern similarity, as well as the intricate interplay between trait anxiety and eCFT generation.

REVIEW ON THE SYNTHESIS OF ALPHA-LIPOIC ACID AND ITS THERAPEUTIC POTENTIAL IN EXPERIMENTAL MODEL OF DEMENTIA

LA or (±)-α-Lipoic acid (6,8-thioctic acid, 5-(1,2-dithiolan-3-yl)pentanoic acid) (LA) is a heterocyclic thia fattyacid consisting of pentanoic acid and a 1,2-dithiolan-3-yl group at the 5-position. LA is an amphiphilic pharmacophorewith excellent antioxidant, anti-inflammatory and neuroprotective effects attested by numerous studies for its potentialutility in both the treatment and diverse forms of prophylaxis of neurodegenerative disorders, especially Alzheimer’sdisease. This article aims to assess the differences in neuroprotective effect after short-term (11 days) and longterm(51 days) LA administration in an experimental rat model of scopolamine-induced dementia by correlatingbiochemical data on acetylcholinesterase activity with behavioural data. Behaviourally appraised changes in learningand memory appear to correlate with biochemical changes in AChE activity. The neuroprotective effect of LA, asascertained by its beneficial effects on learning and memory in a scopolamine animal model, appears to be associatedwith cholinergic mechanisms (a decrease in AChE activity), and to be larger after short-term administration ratherthan long-term administration. These results further underscore the candidacy of LA as a viable drug candidatesuitable for continued investigation and derivate synthesis endeavours.

Post-retrieval stress impairs subsequent memory depending on hippocampal memory trace reinstatement during reactivation.

Upon retrieval, memories can become susceptible to meaningful events, such as stress. Post-retrieval memory changes may be attributed to an alteration of the original memory trace during reactivation-dependent reconsolidation or, alternatively, to the modification of retrieval-related memory traces that impact future remembering. Hence, how post-retrieval memory changes emerge in the human brain is unknown. In a 3-day functional magnetic resonance imaging study, we show that post-retrieval stress impairs subsequent memory depending on the strength of neural reinstatement of the original memory trace during reactivation, driven by the hippocampus and its cross-talk with neocortical representation areas. Comparison of neural patterns during immediate and final memory testing further revealed that successful retrieval was linked to pattern-dissimilarity in controls, suggesting the use of a different trace, whereas stressed participants relied on the original memory representation. These representation changes were again dependent on neocortical reinstatement during reactivation. Our findings show disruptive stress effects on the consolidation of retrieval-related memory traces that support future remembering.

Associations Between Stroke Type, Ischemic Stroke Subtypes, and Post-Stroke Cognitive Trajectories.

It is unclear how post-stroke cognitive trajectories differ by stroke type and ischemic stroke subtype. We studied associations between stroke types (ischemic, hemorrhagic), ischemic stroke subtypes (cardioembolic, large artery atherosclerotic, lacunar/small vessel, cryptogenic/other determined etiology), and post-stroke cognitive decline. This pooled cohort analysis from four US cohort studies (1971-2019) identified 1,143 dementia-free individuals with acute stroke during follow-up: 1,061 (92.8%) ischemic, 82 (7.2%) hemorrhagic, 49.9% female, 30.8% Black. Median age at stroke was 74.1 (IQR, 68.6, 79.3) years. Outcomes were change in global cognition (primary) and changes in executive function and memory (secondary). Outcomes were standardized as T-scores (mean [SD], 50 [10]); a 1-point difference represents a 0.1-SD difference in cognition. Median follow-up for the primary outcome was 6.0 (IQR, 3.2, 9.2) years. Linear mixed-effects models estimated changes in cognition after stroke. On average, the initial post-stroke global cognition score was 50.78 points (95% CI, 49.52, 52.03) in ischemic stroke survivors and did not differ in hemorrhagic stroke survivors (difference, -0.17 points [95% CI, -1.64, 1.30]; P=0.82) after adjusting for demographics and pre-stroke cognition. On average, ischemic stroke survivors showed declines in global cognition, executive function, and memory. Post-stroke declines in global cognition, executive function, and memory did not differ between hemorrhagic and ischemic stroke survivors. 955 ischemic strokes had subtypes: 200 (20.9%) cardioembolic, 77 (8.1%) large artery atherosclerotic, 207 (21.7%) lacunar/small vessel, 471 (49.3%) cryptogenic/other determined etiology. On average, small vessel stroke survivors showed declines in global cognition and memory, but not executive function. Initial post-stroke cognitive scores and cognitive declines did not differ between small vessel survivors and survivors of other ischemic stroke subtypes. Post-stroke vascular risk factor levels did not attenuate associations. Stroke survivors had cognitive decline in multiple domains. Declines did not differ by stroke type or ischemic stroke subtype.

Maternal hypertension alters offspring’s glial cell proportions and behavior

Abstract Preeclampsia (PreE), a hypertensive disorder during pregnancy, is a primary contributor to global obstetric morbidity and mortality. Its effects encompass heightened risks of cognitive impairment and behavior disorders in children born to mothers with PreE. The objective of our study was to determine whether PreE leads to early modifications in the brain's glial cell populations and/or behavioral changes in offspring. To induce PreE, C57BL/6J dams received vasopressin or saline through subcutaneous infusion throughout gestation. Following natural parturition, offspring were euthanized at various postnatal timepoints for glial cell analysis and behavioral evaluation. Flow cytometry was utilized to assess microglia and astrocyte populations. Offspring of PreE pregnancies exhibited decreased total microglia and astrocytes in the brain. Additionally, when compared to offspring from normotensive pregnancies, those born to mothers with PreE displayed impaired performance in the spontaneous alternation Plus-maze task, signifying altered spatial working memory. Our findings substantiate that PreE leads to diminished glial cell populations in offspring postnatally, and these mice exhibit changes in spatial working memory. Continuing research aims to elucidate the influence of PreE on the numbers and functioning of glial cells, along with examining how the compromised numbers and/or functionality of these cells affects the behavior and cognition of offspring born to mothers with PreE.

A Critical Review Based on Preclinical Studies of Medicinal Plants for the Management of Alzheimer’s Disease

Abstract: Alzheimer’s disease (AD) is the most common neurodegenerative and progressive disorder that results in damage to memory and alters thinking and behavior, which represent critical problems the world’s aging population is faced with. Clinical symptoms of AD include cognitive decline, loss of memory, emotional and behavioral changes, loss of motor coordination, and mental impairments. Yet, neither a universally accepted diagnosis with respect to its pathogenesis nor an ideal therapy is available for the management of AD. The existing drugs cause many complications and adverse effects. Herbal drugs, supported by an abundance of traditional knowledge, may fulfill the need as they can target the pathogenesis of AD at various destinations, both at the cellular and molecular levels. In recent years, herbal drugs and formulations have been evaluated in preclinical setups, especially involving rat and mouse models of AD, which have shown their memoryenhancing, neuroprotective, and antioxidant activities. Several herbal drugs and phytochemicals have been evaluated for their effectiveness as antioxidative agents to prevent the occurrence of oxidative stress and ROS formation during AD pathogenesis and exhibit antiapoptotic properties by downregulating caspase-3, DNA fragmentation, NF-κB, interleukin-1 β (IL1β), and TNF levels. In this paper, we have primarily reviewed herbal remedies that have been recently evaluated as alternative treatments for AD in a preclinical setup, and discussed the role of herbal medicines in the management of AD and advances in their knowledge.

Mechanisms of autoimmune encephalitis.

To provide an overview of the pathogenic mechanisms involved in autoimmune encephalitides mediated by antibodies against neuronal surface antigens, with a focus on NMDAR and LGI1 encephalitis. In antibody-mediated encephalitides, binding of IgG antibodies to neuronal surface antigens results in different pathogenic effects depending on the type of antibody, IgG subclass and epitope specificity. NMDAR IgG1 antibodies cause crosslinking and internalization of the target, synaptic and brain circuitry alterations, as well as alterations of NMDAR expressing oligodendrocytes, suggesting a link with white matter lesions observed in MRI studies. LGI1 IgG4 antibodies, instead, induce neuronal dysfunction by disrupting the interaction with cognate proteins and altering AMPAR-mediated signaling. In-vitro findings have been corroborated by memory and behavioral changes in animal models obtained by passive transfer of patients' antibodies or active immunization. These models have been fundamental to identify targets for innovative therapeutic strategies, aimed at counteracting or preventing antibody effects, such as the use of soluble ephrin-B2, NMDAR modulators (e.g., pregnenolone, SGE-301) or chimeric autoantibody receptor T cells (CAART) in models of NMDAR encephalitis. A deep understanding of the pathogenic mechanisms underlying antibody-mediated encephalitides is crucial for the development of new therapeutic approaches targeting brain autoimmunity.

Cannabis sativa Boosts Brain Functions and Ameliorate Anxiety, when used Sensibly and not Abusively

Cannabis sativa is an illegal substance with documented analgesic, antipyretic, anti-inflammatory, and anti-diarrheal properties. Numerous other cannabinoids found in cannabis have an impact on brain activity. So, the purpose of this study was to examine how cannabis sativa extract affected the cognito-motor activity in rats. Twenty-four (24) Wistar rats weighing between 80.53 and 100.49g were randomly divided into four groups (A, B, C, and D) of six animals each after a 14-day acclimatization period to laboratory conditions. Only food and water were provided to Group A. Groups B and C received an oral ethanolic extract of Cannabis sativa at doses of 400 mg/kg and 800 mg/kg, respectively. Group D received an intraperitoneal dose of diazepam at a rate of 50 mg/kg. To ascertain the impact of the cannabis sativa extract on the neuro behavior of the rats, each animal in the four groups is subjected to an experimental test following each administration of the extract (the Barnes maze test, the beam walk test, and the inverted screen tests). The rats in groups B and C that received cannabis sativa extract showed a notable improvement in learning and memory, and the majority of the rats in group C who received cannabis sativa extract walked upright without stumbling. Group A, the control group, exhibited indicators of anxiety and panic but no discernible change in learning or memory. Due to muscle weakness, members of group D (standard drug group) were essentially inactive throughout the experiment, staggering and falling. It can be concluded that cannabis sativa's ethanolic leaf extract is not harmful, boosts brain functions, and promotes learning and memory when used sensibly and not abusively. Thus, it can be inferred that the plant may help with the treatment of several mental health conditions, such as anxiety.

Does Neighborhood Socioeconomic Status Alter Memory Change Associated with a Cancer Diagnosis? Preliminary Evidence from the US Health and Retirement Study.

Neighborhood disadvantage has been linked to cognitive impairment, but little is known about the effect of neighborhood disadvantage on long-term cancer-related memory decline. Incident cancer diagnosis and memory (immediate and delayed recall, combined with proxy-reported memory) were assessed at biennial interviews in the US Health and Retirement Study (N = 13,293, 1998-2016). Neighborhood disadvantage was measured using the National Neighborhood Data Archive disadvantage index, categorized into tertiles (T1: least disadvantaged-T3: most disadvantaged). Linear mixed-effects models estimated the standardized memory trajectories in participants with or without cancer, by neighborhood disadvantage. Living in more disadvantaged neighborhoods was associated with worse mean memory function and steeper memory declines, regardless of cancer status. An incident cancer diagnosis was associated with an acute memory drop for those living in least disadvantaged neighborhoods but not more disadvantaged neighborhoods [T1: -0.05, 95% confidence interval (CI): -0.08, -0.01; T3: -0.13, 95% CI: -0.06, 0.03]. Cancer survivors in the least disadvantaged neighborhoods had a slight memory advantage in the years prior to diagnosis (T1: 0.09, 95% CI: 0.04, 0.13) and after diagnosis (T1: 0.07, 95% CI: 0.01, 0.13). An incident cancer diagnosis among those living in the least disadvantaged neighborhoods was associated with an acute memory drop at the time of diagnosis and a long-term memory advantage before and after diagnosis compared with cancer-free individuals in similar neighborhoods. These findings could inform interventions to promote cancer survivor's long-term aging. Future studies should investigate the social and biological pathways through which neighborhood socioeconomic status could influence cancer-related memory changes.

Free water-corrected fractional anisotropy of the fornix and parahippocampal cingulum predicts longitudinal memory change in cognitively healthy older adults

Prior studies have reported inconsistent results regarding the relationships between the integrity of the fornix and parahippocampal cingulum and both memory performance and longitudinal change in performance. In the present study, we examined associations in a sample of cognitively healthy older adults between free water-corrected fractional anisotropy (FA) metrics derived from the fornix and cingulum, baseline memory performance, and 3-year memory change. Neither fornix nor cingulum FA correlated with memory performance at baseline. By contrast, FA of each tract was predictive of memory change, such that greater FA was associated with less longitudinal decline. These associations remained significant after controlling for FA of other white matter tracts and for performance in other cognitive domains. Furthermore, fornix and cingulum FA explained unique variance in memory change. These results suggest that free water-corrected measures of fornix and parahippocampal cingulum integrity are reliable predictors of future memory change in cognitively healthy older adults. The findings for the fornix in particular highlight the utility of correcting for free water when estimating diffusion tensor imaging metrics of white matter integrity.

Evidence of an active role of dreaming in emotional memory processing shows that we dream to forget

Dreaming is a universal human behavior that has inspired searches for meaning across many disciplines including art, psychology, religion, and politics, yet its function remains poorly understood. Given the suggested role of sleep in emotional memory processing, we investigated whether reported overnight dreaming and dream content are associated with sleep-dependent changes in emotional memory and reactivity, and whether dreaming plays an active or passive role. Participants completed an emotional picture task before and after a full night of sleep and they recorded the presence and content of their dreams upon waking in the morning. The results replicated the emotional memory trade-off (negative images maintained at the cost of neutral memories), but only in those who reported dreaming (Dream-Recallers), and not in Non-Dream-Recallers. Results also replicated sleep-dependent reductions in emotional reactivity, but only in Dream-Recallers, not in Non-Dream-Recallers. Additionally, the more positive the dream report, the more positive the next-day emotional reactivity is compared to the night before. These findings implicate an active role for dreaming in overnight emotional memory processing and suggest a mechanistic framework whereby dreaming may enhance salient emotional experiences via the forgetting of less relevant information.

Ozanimod Differentially Impacts Circulating Lymphocyte Subsets in Patients with Moderately to Severely Active Crohn’s Disease

BackgroundOzanimod showed efficacy and safety in the phase 2 STEPSTONE study conducted in patients with moderately to severely active Crohn’s disease.AimsThis analysis assessed the effects of ozanimod on circulating lymphocytes in Crohn’s disease.MethodsPatients received ozanimod 0.92 mg for 12 weeks. Lymphocyte subtypes were evaluated using multicolor flow analysis on blood samples collected before treatment and on Week 12. Absolute lymphocyte count changes were analyzed by Wilcoxon signed rank tests. Disease activity changes and efficacy outcomes were evaluated at Week 12, and associations with lymphocyte subtype levels were assessed using Spearman’s correlation and logistic regression.ResultsReductions in median total T, Th, and cytotoxic T cells occurred at Week 12 (45.4%–76.8%), with reductions in most subtypes of 47.5% to 91.3% (P < 0.001). CD8+ terminally differentiated effector memory cells were largely unaffected (median change, − 19%; P = 0.44). Reductions in median total B cells occurred at Week 12 (76.7%), with reductions in subtypes of 71.4% to 81.7% (P < 0.001). Natural killer and monocyte cell counts were unchanged. Greater baseline levels and changes in nonswitched memory B cells were significantly associated with clinical, endoscopic, and histologic efficacy (P < 0.05, all comparisons).ConclusionsOzanimod reduced circulating levels of all B-cell and most T-cell subsets but not monocytes or natural killer cells. Key subsets relevant to immune surveillance were not reduced, supporting the low risk of infection and malignancy with ozanimod in chronic inflammatory diseases. Levels of nonswitched memory B cells were associated with efficacy, providing a potential marker for ozanimod response.Trial Registration ClinicalTrials.gov: NCT02531113, EudraCT: 2015–002025–19Graphical

Relationships between trace elements and cognitive and depressive behaviors in sprague dawley and wistar albino rats.

Introduction: This study investigates the effects of social isolation on mental health and cognitive functions in Sprague Dawley (SD) and Wistar Albino (WIS) rat strains, prompted by the heightened awareness of such impacts amid the COVID-19 pandemic. This study aims to explore the impact of social isolation on memory, learning, and behavioral changes in middle-aged SD and WIS rat strains and to investigate cortical trace element levels, seeking potential correlations between these levels and the observed behavioral responses to social isolation. Methods: Four groups of 14-month-old male rats were established: control and isolated SDs and WIS rats (CONT-SD, ISO-SD, CONT-WIS, ISO-WIS). Morris Water Maze and Porsolt Forced Swimming tests were conducted for behavioral assessment. Following behavioral tests, rats were sacrificed under general anesthesia, and cortices were isolated for analysis of macro and trace element levels (ICP/MS). Results: In behavioral tests, CONT-SD rats exhibited superior performance in the Morris Water Maze test compared to CONT-WIS rats, but displayed increased depressive behaviors following social isolation, as evident in the Porsolt Forced Swimming test (p < 0.05). ISO-SD rats showed elevated levels of Co and Cu, along with reduced levels of Cs and As, compared to ISO-WIS rats. Moreover, isolation resulted in decreased Cu and Mo levels but increased Rb levels in WIS rats. Comparison of trace element levels in naïve groups from different strains revealed lower Zn levels in the WIS group compared to SD rats. Discussion: The findings suggest that the SD strain learns faster, but is more susceptible to depression after isolation compared to the WIS strain. Increased Co and Cu levels in ISO-SD align with previous findings, indicating potential trace element involvement in stress responses. Understanding these mechanisms could pave the way for preventive treatment strategies or therapeutic targets against the consequences of stressors, contributing to research and measures promoting a balanced diet to mitigate neurobehavioral abnormalities associated with social isolation in the future.

Web-based cognitive rehabilitation intervention for cancer-related cognitive impairment following chemotherapy for aggressive lymphoma: protocol for a randomised pilot trial

IntroductionCancer-related cognitive impairment is common among people diagnosed with and treated for cancer. This can be a distressing and disabling side effect for impacted individuals. Interventions to mitigate cognitive dysfunction...

Structural white matter properties and cognitive resilience to tau pathology.

We assessed whether macro- and/or micro-structural white matter properties are associated with cognitive resilience to Alzheimer's disease pathology years prior to clinical onset. We examined whether global efficiency, an indicator of communication efficiency in brain networks, and diffusion measurements within the limbic network and default mode network moderate the association between amyloid-β/tau pathology and cognitive decline. We also investigated whether demographic and health/risk factors are associated with white matter properties. Higher global efficiency of the limbic network, as well as free-water corrected diffusion measures within the tracts of both networks, attenuated the impact of tau pathology on memory decline. Education, age, sex, white matter hyperintensities, and vascular risk factors were associated with white matter properties of both networks. White matter can influence cognitive resilience against tau pathology, and promoting education and vascular health may enhance optimal white matter properties. Aβ and tau were associated with longitudinal memory change over ∼7.5 years. White matter properties attenuated the impact of tau pathology on memory change. Health/risk factors were associated with white matter properties.

Autobiographical memory following weight gain in adult patients with Anorexia Nervosa: A longitudinal study.

Patients with anorexia nervosa (AN) show overgeneralization of memory (OGM) when generating autobiographical episodes related to food and body shape. These memories are central for the construction of a coherent self-concept, interpersonal relationships, and problem-solving abilities. The current study aims to investigate changes in autobiographical memory following weight gain. OGM was assessed with an adapted version of the Autobiographical Memory Test including food-, body-, depression-related, and neutral cues. N=41 female patients with AN (28 restricting-, 13 binge-eating/purging-subtype; mean disease duration: 4.5years; mean BMI: 14.5kg/m2) and N=27 healthy controls (HC) were included at baseline. After inpatient treatment (mean duration: 11weeks), 24 patients with AN and 24 age-matched HC were reassessed. Group differences were assessed using independent samples t-tests for cross-sectional comparisons and repeated measures ANOVAs for longitudinal data. At baseline, patients with AN generated significantly fewer specific memories than HC, independent of word category (F(1.66)=27.167, p<0.001). During inpatient stay, the average weight gain of patients with AN was 3.1 body mass index points. At follow-up, patients with AN showed a significant improvement in the number of specific memories for both depression-related and neutral cues, but not for food- and body-related cues. Generalised OGM (i.e., independent of word category) in patients with AN before weight restoration may be a general incapacity to recall autobiographical memory. After weight gain, the previously well-studied pattern of eating disorder-related OGM emerges. The clinical relevance of the continuing disorder-related OGM in patients with AN after weight gain is discussed.

Causal functional maps of brain rhythms in working memory

Human working memory is a key cognitive process that engages multiple functional anatomical nodes across the brain. Despite a plethora of correlative neuroimaging evidence regarding the working memory architecture, our understanding of critical hubs causally controlling overall performance is incomplete. Causal interpretation requires cognitive testing following safe, temporal, and controllable neuromodulation of specific functional anatomical nodes. Such experiments became available in healthy humans with the advance of transcranial alternating current stimulation (tACS). Here, we synthesize findings of 28 placebo-controlled studies (in total, 1,057 participants) that applied frequency-specific noninvasive stimulation of neural oscillations and examined working memory performance in neurotypical adults. We use a computational meta-modeling method to simulate each intervention in realistic virtual brains and test reported behavioral outcomes against the stimulation-induced electric fields in different brain nodes. Our results show that stimulating anterior frontal and medial temporal theta oscillations and occipitoparietal gamma rhythms leads to significant dose-dependent improvement in working memory task performance. Conversely, prefrontal gamma modulation is detrimental to performance. Moreover, we found distinct spatial expression of theta subbands, where working memory changes followed orbitofrontal high-theta modulation and medial temporal low-theta modulation. Finally, all these results are driven by changes in working memory accuracy rather than processing time measures. These findings provide a fresh view of the working memory mechanisms, complementary to neuroimaging research, and propose hypothesis-driven targets for the clinical treatment of working memory deficits.