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At least 19 recordsLinked to original sources

PubMed2026

Development and Validation of a Predictive Model for Identification of Cognitive Impairment Risk in Older Adults with Subjective Cognitive Decline：A Longitudinal Study.

BACKGROUND: Subjective cognitive decline (SCD) is a transitional state between objective cognitive impairment and cognitively intact mental status, providing a critical window for implementing preventive interventions to delay objective cognitive decline. AIMS: We aimed to develop a predictive model for SCD progression in older adults with mild cognitive impairment (MCI). This model will facilitate the identification of risk factors and establishment of targeted interventions for community-based SCD management. METHODS: Data from the China Health and Retirement Longitudinal Study (CHARLS) was utilized in this study, extracting 18 indicators. Potential predictors selected through univariate Cox regression and LASSO regression analyses were sequentially incorporated into a multivariable Cox regression model. A nomogram was constructed to establish a predictive model. Model validation encompassed Area Under Curve (AUC) metrics for discriminative capacity, complemented by quantitative assessments using calibration curve analysis for precision verification and decision curve analysis (DCA) for clinical utility evaluation. RESULTS: A total of 1099 older adults with SCD were included in the final analysis, of whom 114 (10.3%) developed MCI. Multivariable Cox regression identified residence, marital status, educational level, social participation, gait speed, and baseline cognitive function. The model demonstrated time-dependent AUC values of 0.885, 0.830, 0.839, and 0.836 in the training set when evaluating discriminative capacity at 2-, 4-, 7-, and 9-year, respectively. The predictive model showed excellent predictive ability according to AUC, calibration curve, and DCA. CONCLUSIONS: A predictive model was created to estimate the risk of developing MCI in older individuals with SCD, offering clinician-actionable intervention benchmarks for preventive care.

Humans↗

PubMed2025

Whole-genome Sequence Analysis Revealed Novel Subjective Cognitive Decline-associated Genes in 10,763 Chinese.

Subjective cognitive decline (SCD) is widely regarded as a potential preclinical stage of Alzheimer's disease (AD), yet its genetic basis remains poorly understood. To address this gap, we investigated genetic biomarkers associated with SCD using whole-genome sequencing (WGS) in 10,763 Chinese participants from the Healthy Zhejiang One Million People Cohort (HOPE Cohort). The discovery stage included 9284 samples, with 1479 samples used for validation. Using a two-stage design, we systematically investigated both common and rare variants associated with SCD. In rare variant analyses, we identified and replicated an association between the upstream region of SEPHS2 and SCD. SEPHS2 is involved in selenophosphate synthesis, and a Mendelian randomization analysis reveals that its expression levels in both blood and brain cerebellum are associated with AD. Additionally, we identified CLVS2, which encodes a protein primarily expressed in neuronal cells, as a potential regulator for SCD based on missense rare variants. Multi-omics evidence suggests that both SEPHS2 and CLVS2 may play roles in neurodegenerative diseases. For common variants, we validated 8 known loci related to cognitive decline, 3 of which originated from the only existing SCD genetic study conducted under a migraine background. Overall, our WGS-based study fills the gap in SCD research by providing vital genetic evidence from an East Asian population and offers insights into the pathogenic mechanisms of SCD.

Aged↗

PubMed2026

Subjective cognition trajectories, Alzheimer biomarkers, and incident mild cognitive impairment.

BACKGROUND: Subjective cognitive decline is common in older adults and may represent an early clinical signal along the Alzheimer's disease continuum. The clinical relevance of longitudinal changes in subjective cognitive decline remains unclear. OBJECTIVES: To determine whether trajectories of self- or study partner-reported cognitive decline predict progression to mild cognitive impairment and reflect Alzheimer's disease-specific biological patterns. DESIGN, SETTING, PARTICIPANTS: Data were pooled from two observational cohorts. Cognitively unimpaired participants with baseline amyloid status, repeated assessments of subjective cognitive decline, and clinical follow-up were included. The study included 770 participants with a median follow-up of 5.0 years (interquartile range 4.0-7.0). MEASUREMENTS: Subjective cognitive decline was assessed using the Everyday Cognition questionnaire completed by participants and study partners. Linear mixed-effects models examined associations with amyloid status and progression to mild cognitive impairment. Cox proportional hazards models tested whether one-year changes predicted progression. RESULTS: Amyloid-positive participants and those who progressed to mild cognitive impairment showed steeper increases in self- and study partner-reported cognitive difficulties over time. Among amyloid-positive participants, only increases in study partner-report differentiated progressors from non-progressors. One-year increases in study partner-report predicted a higher risk of mild cognitive impairment compared with unchanged scores (hazard ratio 3.24; 95% confidence interval 1.73-6.07]), with effects confined to amyloid-positive participants. CONCLUSIONS: Short-term increases in study partner-reported cognitive difficulties identify amyloid-positive cognitively unimpaired older adults at increased risk of near-term progression to mild cognitive impairment. Longitudinal monitoring using study partner reports may provide a low-burden and clinically relevant approach for early risk stratification and surveillance in aging populations.

Humans↗

PubMed2026

Effectiveness of psychosocial and lifestyle interventions in promoting behaviour change and improving cognitive outcomes in older people with memory concerns: A systematic review.

BACKGROUND: Older adults with mild cognitive impairment or subjective cognitive decline have a greater dementia risk, particularly those from minority ethnic and socioeconomically disadvantaged backgrounds. Psychosocial and lifestyle interventions targeting modifiable risk factors offer hope for reducing risk, yet behavioural mechanisms remain unclear. This systematic review examines these mechanisms and associated outcomes. METHOD: We searched PubMed, Embase (Ovid), PsycINFO (Ovid), Web of Science, and Scopus for randomised control trials testing interventions that aimed to improve lifestyle and cognition in older adults with memory concerns. We explored behavioural mechanisms using the COM-B model and synthesised intervention effectiveness, overall and within underserved groups. We prioritised lower risk of bias studies. RESULTS: 26 studies described 23 randomised controlled trials (14 multidomain, 9 single domain interventions). Certainty of evidence that behaviour change was associated with cognition was low. Moderate-certainty evidence indicated that interventions providing a socially supportive environment and combining nutritional education and counselling for 6 + months improved diet. Physical activity improved primarily in interventions incorporating education, structured training, and enablement strategies (e.g., tailored programmes, providing tools). Interventions simultaneously targeting capability, opportunity and motivation showed greater overall effectiveness. Few studies recorded ethnicity (13%) or sociodemographic status (9%), and none explored their impact. CONCLUSIONS: Non-pharmacological interventions can help this population improve their lifestyles if they feel capable, equipped and motivated, highlighting the value of careful design and implementation. There is scarce evidence on how these interventions work for underserved populations. Future research should explore this to inform tailored interventions and develop equitable dementia prevention strategies.

Humans↗

PubMed2026

Age at menopause and subjective cognitive symptoms predict digital cognitive outcomes at the gynecological Well-Woman visit.

INTRODUCTION: Women are at increased risk for Alzheimer's Disease (AD). Growing evidence suggests that the menopausal transition may represent a vulnerable window for development of AD-related pathology. Yet, women are diagnosed with AD later than men. Conducting routine cognitive screenings and integrating information about both cognitive symptoms and age at menopause may help address sex-based disparities in detection and prevention. This study investigated whether subjective cognitive symptoms, in combination with age at menopause, were associated with performance on a digital cognitive task in postmenopausal women. METHODS: 183 postmenopausal women (mean age = 63.8, range = 45-85) were recruited after their Well-Woman visit. Participants completed the Screener for Cognitive Problems in Everyday Life (SCoPE) to assess subjective cognitive symptoms, followed by a sensitive measure of objective cognition: the Linus Health Digital Clock and Recall (DCR™). Information was also collected on age at menopause. We examined associations of subjective cognitive symptoms and age at menopause with digital cognitive performance, adjusting for age, education and depression. Model fit was evaluated using adjusted R2, AIC, and BIC. RESULTS: 48.1% of women reported one or more cognitive symptoms on the SCoPE. On objective testing, 73.2% scored in the normal range, 20.8% in the borderline range, and 6.0% in the impaired range. SCoPE total score was negatively associated with objective cognitive performance in adjusted models (B = -.12, p = .03). Age at menopause showed a significant quadratic association with cognitive performance (B = -0.006, p<.001). SCoPE total was not associated with DCR subtests, while age at menopause predicted both Delayed Recall and Clock Drawing. CONCLUSION: Subjective cognitive symptoms and age at menopause were associated with lower performance on a sensitive, objective cognitive test. Findings support routine cognitive screening and suggest that subjective cognitive symptoms as well as age at menopause are associated with cognitive function.

Humans↗

PubMed2022

Improving risk indexes for Alzheimer's disease and related dementias for use in midlife.

Knowledge of a person's risk for Alzheimer's disease and related dementias (ADRDs) is required to triage candidates for preventive interventions, surveillance, and treatment trials. ADRD risk indexes exist for this purpose, but each includes only a subset of known risk factors. Information missing from published indexes could improve risk prediction. In the Dunedin Study of a population-representative New Zealand-based birth cohort followed to midlife (N = 938, 49.5% female), we compared associations of four leading risk indexes with midlife antecedents of ADRD against a novel benchmark index comprised of nearly all known ADRD risk factors, the Dunedin ADRD Risk Benchmark (DunedinARB). Existing indexes included the Cardiovascular Risk Factors, Aging, and Dementia index (CAIDE), LIfestyle for BRAin health index (LIBRA), Australian National University Alzheimer's Disease Risk Index (ANU-ADRI), and risks selected by the Lancet Commission on Dementia. The Dunedin benchmark was comprised of 48 separate indicators of risk organized into 10 conceptually distinct risk domains. Midlife antecedents of ADRD treated as outcome measures included age-45 measures of brain structural integrity [magnetic resonance imaging-assessed: (i) machine-learning-algorithm-estimated brain age, (ii) log-transformed volume of white matter hyperintensities, and (iii) mean grey matter volume of the hippocampus] and measures of brain functional integrity [(i) objective cognitive function assessed via the Wechsler Adult Intelligence Scale-IV, (ii) subjective problems in everyday cognitive function, and (iii) objective cognitive decline measured as residualized change in cognitive scores from childhood to midlife on matched Weschler Intelligence scales]. All indexes were quantitatively distributed and proved informative about midlife antecedents of ADRD, including algorithm-estimated brain age (β's from 0.16 to 0.22), white matter hyperintensities volume (β's from 0.16 to 0.19), hippocampal volume (β's from -0.08 to -0.11), tested cognitive deficits (β's from -0.36 to -0.49), everyday cognitive problems (β's from 0.14 to 0.38), and longitudinal cognitive decline (β's from -0.18 to -0.26). Existing indexes compared favourably to the comprehensive benchmark in their association with the brain structural integrity measures but were outperformed in their association with the functional integrity measures, particularly subjective cognitive problems and tested cognitive decline. Results indicated that existing indexes could be improved with targeted additions, particularly of measures assessing socioeconomic status, physical and sensory function, epigenetic aging, and subjective overall health. Existing premorbid ADRD risk indexes perform well in identifying linear gradients of risk among members of the general population at midlife, even when they include only a small subset of potential risk factors. They could be improved, however, with targeted additions to more holistically capture the different facets of risk for this multiply determined, age-related disease.

Alzheimer’s disease↗

PubMed1977

Effects of instructions, biofeedback, and cognitive activities on heart rate control.

In a factorial experiment, 90 male and 90 female subjects were given (a) either instructions to increase heart rate (HR), decrease HR, or no instructions to change their HR; (b) either true biofeedback, false biofeedback, or no biofeedback; and (c) either instructions concerning cognitions to help them change HR or no instructions concerning cognitions. The results indicated that (a) for increasing HR, instructions to increase HR were as effective as the combination of instructions and true biofeedback; (b) for decreasing HR, neither instructions nor biofeedback nor the combination of instructions and biofeedback was more effective than simply sitting quietly; (c) although subjects instructed to increase HR showed higher HRs at the end of training than subjects instructed to decrease, the increase subjects showed a decline in HR from the initial period; (d) almost all subjects reported using cognitions to influence HR, and instructions concerning the use of cognitions did not facilitate changes in HR; and (e) women showed higher HRs, which declined more slowly than those of men, but sex did not interact with any treatment variable. It was concluded that increases (or retarded decreases) in HR were due to instructions, and decreases were due to simple adaptation, thus raising serious questions concerning the effectiveness of the biofeedback component of "biofeedback training" for altering HR.

Biofeedback, Psychology↗

PubMed2025

Altered mitochondrial DNA methylation in blood in individuals with mild cognitive impairment.

BACKGROUND: Previous studies reported that altered mitochondrial methylation in Alzheimer's disease (AD), however, whether epigenetic modifications in mitochondrial genomes contribute to preclinical AD remains unclear. This study aimed to investigate mitochondrial methylation changes in individuals with cognitive decline. RESEARCH DESIGN AND METHODS: We examined whole mitochondrial genome methylation in 50 individuals with mild cognitive impairment (MCI) and 50 individuals without MCI, using bisulfite amplicon sequencing, assessing methylation at 366 Cytosine-guanine oligodeoxynucleotide (CpG) sites. RESULTS: We found the overall methylation level of mitochondrial DNA (mtDNA) in each subject was relatively low, ranging from 0% to 15%. Global methylation was significantly higher in individuals with cognitive decline compared to controls (3.86% vs. 3.46%, p = 0.037), with 34 differentially methylated CpG sites identified. Methylation differences (MD) between cognitive decline individuals and controls were 22.93 ± 5.60% at chrM6465 (Q = 0.013), 12.55 ± 3.02% at chrM9612 (Q = 0.013), 11.45 ± 3.88% at chrM11762 (Q = 0.159) and 11.03 ± 3.88% at chrM11766 (Q = 0.172), respectively, while the level of MD at chrM15812 was -13.11 ± 4.31% (Q = 0.159) after Benjamini-Hochberg FDR adjusted. Furthermore, Methylation at specific sites were significantly correlated with Mini-Mental State Examination scores, distinguishing individuals with cognitive decline from controls. CONCLUSIONS: Our study provides an mtDNA methylation map and suggests a role for these sites in preclinical AD pathogenesis.

Humans↗

PubMed1976

Age differences in humor comprehension and appreciation in old age.

Ninety-six subjects in three age groups (50-59, 60-69, 70-79) who resided at home were tested on their appreciation and comprehension of 12 conservation and 12 nonconservation jokes. The conservation jokes depended on the Piagetian concepts of conservation of mass, weight, and volume for their comprehension. Cognitive ability of the subjects on the three conservation tasks was also tested. Appreciation increased with age and comprehension decreased with age for both types of jokes. The ability to conserve volume declined with age. Among conservers of volume, appreciation of conservation of volume jokes increased with age; among nonconservers, it tended to decrease. The study provided some support to the hypothesis that the cognitive perceptual theory of humor applies in old age as it does in childhood, with appreciation depending on a match between ability level and the cognitive demand of the joke.

Aged↗

PubMed1976

Relations of age and personality dimensions to cognitive ability factors.

The relation between three cognitive ability factors - Information Processing Ability (IPA), Manual Dexterity (MD), and Pattern Analysis Capability (PAC) - and three personality dimensions - Anxiety, Extraversion, and Openness to Experience - were examined in three age groups. Subjects were 969 male volunteers ranging in age from 25 to 82. Subjects high in anixety scored lower on all three cognitive factors; subjects open to experience scored higher on IPA and PAC; and introverted subjects scored higher on PAC. Most of these effects remained when the education and socio-economic status were held constant in covariance analyses. Older subjects performed less well than younger ones on MD and PAC, but not on IPA. While personality has some influence on cognitive performance, the declines with age in performance on some cognitive tasks are not mediated by personality.

Adult↗

PubMed1976

Reaction time as a diagnostic measure in senility.

Both simple and disjunctive reaction times (RT) are known to slow with aging but there is a paucity of information on RT changes in senility. Since disjunctive RT involves cognition in addition to the sensory-motor speed and attentional components of simple RT, it was hypothesized that disjunctive RT would be a reliable index of age-related mental decline. To test this prediction, simple and disjunctive RT were measured in matched groups of 20 normal and 20 cognitively impaired elderly. Simple RT was slower in the senile patients than in the normal subjects, but this difference was accounted for by differences in disjunctive RT. The senile patients showed a much larger performance decrement with respect to disjunctive RT than did the normal subjects--a difference which was not accounted for by differences in simple RT. In a discriminant function analysis, disjunctive RT alone correctly identified the senile patients and the normal subjects with 86% accuracy. Thus, this measure proved to be a reliable index of age-related mental decline. Preliminary data indicate that disjunctive RT slowing is correlated with non-memory mental decline, and that poor performance is related to the need for care and supervision.

Adult↗

PubMed2025

GHSR suppression in neurons protects against aging-associated metabolic and cognitive impairments.

Aging is accompanied by progressive declines in metabolic and cognitive functions. Growth hormone secretagogue receptor (GHSR), a receptor for the gut hormone ghrelin, is highly expressed in neurons and plays a crucial role in metabolic regulation. We previously reported that aged global GHSR-ablated mice are lean and insulin-sensitive, and that neuronal GHSR-deleted mice (Syn1-cre;Ghsrf/f) completely prevent diet-induced obesity. However, the role of neuronal GHSR in metabolic and cognitive aging has not been elucidated. The current study aims to determine the roles of neuronal GHSR in aging metabolism and cognitive dysfunction. Syn1-cre;Ghsrf/f mice were subjected to cold stress, glucose- and insulin-tolerance tests, behavioral tests, and tissue analysis. Aging is accompanied by glycemic dysregulation and insulin resistance; old Syn1-cre;Ghsrf/f mice showed improved glucose tolerance and insulin sensitivity. Aging is associated with thermogenic impairment and cognitive decline; old Syn1-cre;Ghsrf/f mice showed better cold resistance and retained better recognition memory. Noticeably, there were increased expression of thermogenic makers (PGC1α and UCP1) and elevated sympathetic innervation markers (tyrosine hydroxylase and synaptophysin) in brown adipose tissue of old Syn1-cre;Ghsrf/f mice. Lastly, old Syn1-cre;Ghsrf/f mice exhibited decreased pro-inflammatory cytokines and increased neural plasticity-related markers (brain-derived neurotrophic factor, synaptophysin, and tyrosine hydroxylase) in metabolic and cognitive-relevant brain regions such as hypothalamus, cortex, and hippocampus. In conclusion, neuronal inhibition of GHSR promotes a healthy aging phenotype showing improved energy metabolism and cognitive function, which is likely contributed to the improved thermogenesis and insulin sensitivity, reduced inflammation, and restored neuronal plasticity.

Animals↗

PubMed1975

Auditory and visual memory losses in aging populations.

Seventy-four men and women (age range, 44-77 years) were tested for short-term auditory and visual memory as part of a larger series of memory and cognitive function tests. All test scores for visual memory, including facial photograph recognition when a sequence requirement was adhered to, showed a significant decline (p smaller than .05) in a comparison of subjects aged 44-54 and subjects aged 55-64. This decline was not observed with the two tests of auditory memory. Thus the data indicate that short-term visual memory may be more susceptible to aging than is auditory memory.

Adult↗

PubMed1976

Age differences in cognition in healthy educated men: a factor analysis of experimental measures.

Performance measures for a wide variety of cognitive laboratory tasks were factor analyzed, and the factors were identifiable as aspects of cognitive processing. The sample consisted of 96 healthy, educated men whose ages ranged from 20 to 80 yr. The factors were identified as speed of information processing, secondary memory, attention, and primary processing efficiency. Factor scores for each factor were correlated with age; r = -0.35, -0.30, -0.40, and -0.15 respectively, with better performance associated with lower age. The sample was divided into subsamples of 32 young (20-39), 32 middle (40-59), and 32 old (60-80) subjects; and each subsample was factor-analyzed separately to determine whether the factor structure was similar for all age groups. Evidence for factor-structure invariance with adult age was found in that all four factors in the primary analysis were identifiable in each of the age subsamples. The findings are consistent with a model of continual cognitive decline with age in healthy, educated adult males.

Adult↗

PubMed2026

Urban Design Quality and Clinical Mental Health: A Systematic Review.

ObjectivesThis systematic review synthesizes empirical evidence on core urban design dimensions that affect clinical mental health outcomes and examines how environmental exposures mediate or moderate these relationships.BackgroundUrban design has increasingly been recognized as a determinant of psychological well-being, yet a standardized framework to evaluate its mental health impact remains underdeveloped.MethodsFollowing PRISMA 2020 guidelines, we systematically reviewed 19 quantitative empirical studies published through January 2025, examining relationships between outdoor urban design features and validated clinical mental health indicators across four major databases.ResultsFindings reveal that urban design influences clinical mental health outcomes (depression, anxiety, stress, cognitive decline) through two objective spatial scales: street-level features (imageability, enclosure, human scale, complexity) and neighborhood environments (land use mix, density, green infrastructure). Environmental exposures (traffic, noise, air pollution) operate as perceptual and experiential mechanisms that mediate or moderate the mental health effects of these spatial design features.ConclusionsWe propose an integrated three-domain conceptual framework distinguishing objective spatial design scales from subjective exposure mechanisms. This framework provides evidence-based guidance for urban planners and policymakers toward creating mentally healthier urban environments.

Humans↗

PubMed1976

The effects of changing the phase and duration of sleep.

The relative effects of extended sleep, reduced sleep, and shifts of habitual sleep time on subsequent performance and mood were studied. Ten healthy male university students who regularly sleep 9.5-10.5 hr were the subjects. Measurements were obtained from a 45-min auditory vigilance task, a 5-min experimenter-paced addition task and a mood adjective check list 30 min after awakening, at midday, and in the evening following five electroencephalographically recorded nights of sleep. The experimental treatments compromised at 9.5-10.5 hr habitual sleep condition and four conditions in which the regular sleep period was lengthened, reduced, delayed, and advanced by 3hr. Following each 3-hr altered condition of sleep there was an equivalent decline in vigilance performance and in subjective arousal as measured by the mood scales. Together with other recent evidence, the present results support the hypothesis that acute disruption of the 24-hr sleep-wakefulness cycle produces degradations in human performance largely independent of total sleep time.

Arousal↗

PubMed1979

Cardiorespiratory health, reaction time and aging.

Visual simple and choice reaction time (RT) tests were administered to 64 male and female volunteers 23 to 59 years of age. One half of the subjects were runners involved in rigorous training programs averaging 42 miles per week. The other half of the subjects were sedentary adults. Eighty simple and 100 choice reaction time trials were given with a variable foreperiod ranging from 400 to 1100 msec. Five catch trials were given in both simple and choice reaction time conditions. The results indicated that there was a gradual decline in RT performance as age increased. However, this trend was not evident in the trained group. Reaction time remained constant with age within the trained group. It was concluded that a high state of cardiorespiratory training may prevent cognitive decrements in performance with age.

Adult↗

PubMed2026

Systematic Review and Transcriptomic Meta-analysis of Environmental Enrichment Reveal Core Molecular Programs of Brain Plasticity.

Environmental enrichment (EE) paradigms in rodents have long demonstrated that enhanced sensory, cognitive, social, and motor stimulation positively impacts brain function, improving learning, memory, and neuroplasticity. These effects have significant implications for understanding cognitive development and mitigating cognitive decline and brain aging. While numerous transcriptomic studies have explored EE-induced molecular changes, a unified view of the genes and pathways consistently modulated remains lacking. To address this gap, we performed a systematic review and meta-analysis. We conducted a comprehensive PubMed search for all studies published up to February 2025 that matched all the following inclusion criteria: (1) employed EE paradigms; (2) were conducted on rodents; (3) utilized genome-wide transcriptomic methods; (4) examined brain regions or neuronal populations. The 323 retrieved articles were manually screened for relevance to the study aims and data availability. Datasets from 20 eligible RNA-seq reports were reprocessed using a unified analysis pipeline and subjected to a meta-analysis with three complementary statistical methods. Despite considerable heterogeneity across studies, our integrative analysis identified consistent gene expression signatures linked to synaptic function, plasticity and their transcriptional regulation. In particular, our findings highlight the upregulation of the activity-dependent transcriptional program, including Fos and Jun family members. These molecular insights advance our understanding of how EE impacts on neuronal and behavioral outcomes, and may inform therapeutic strategies aimed at replicating or enhancing EE benefits. To promote open science and foster further research, we developed an accessible web application, mEEtaBrain, that enables the neuroscience community to navigate and interrogate our meta-analysis results. Substantial methodological heterogeneity across source studies increased variability in the meta-analysis outcomes. The use of stressors or disease models, particularly in rat studies, introduced a major confounding factor and limited reliable interspecies comparison. Overall, the studies exhibited a low to moderate risk of bias.

Neuronal Plasticity↗