Chinese women experience higher dementia rates than men, yet sex-specific risk factors are understudied. We examined how menopause age affects cognitive function and decline in aging Chinese women.
Data were from 7419 postmenopausal women 45–101 years of age at baseline in the China Health and Retirement Longitudinal Study (CHARLS; 2011–2018). Menopause age was categorized using clinical cutoffs (<40, 40–44, 45–49, 50–55, >55 years). Cognitive function was assessed with neuropsychological tests up to four times over 7 years, and associations were analyzed using multivariable-adjusted linear mixed-effects regression.
Compared to menopause at 50–55 years (3661/7419; 49.3%), premature (<40; 235/7419; 3.2%), early (40–44; 623/7419; 8.4%), and late menopause (>55; 366/7419; 4.9%) were associated with lower baseline cognitive scores. Although the rate of cognitive decline did not differ significantly across menopause age groups, late menopause showed a trend toward faster decline.
Cognitive health interventions should consider extreme menopausal age as a risk factor.
Tau pathology impacts neurodegeneration and cognitive decline in Alzheimer's disease (AD), with the dorsal raphe nucleus (DRN) being among the brain regions showing the earliest tau pathology. As a serotonergic hub, DRN activity is altered by selective serotonin reuptake inhibitors (SSRIs), which also have variable effects on cognitive decline and pathology in AD.
We examined N = 191 subjects with baseline 18F-fluorodeoxyglucose positron emission tomography and plasma biomarker data to study the effects of SSRIs on tau pathology, cognitive decline, and DRN metabolism.
Plasma phosphorylated tau 181 (p-tau181) was lower with SSRI use. The effect of SSRIs on cognition varied by cognitive assessment. The DRN was hypometabolic in AD patients relative to healthy controls; however, SSRI use restored the metabolic activity of this region in AD patients.
Long-term SSRI use may reduce the pathological presentation of AD but has variable effects on cognitive performance.
The characteristic events in neurodegenerative diseases (NDDs) encompass protein misfolding, aggregation, accumulation, and their related cellular dysfunction, synaptic function loss. While distinct proteins are implicated in the pathological processes of different NDDs, the process of protein misfolding and aggregation remains notably similar across various conditions. Specifically, proteins undergo misfolding into beta-folded (β-folded) conformation, resulting in the formation of insoluble amyloid proteins. Despite advancements in comprehending protein aggregation, certain facets of this intricate process remain incompletely elucidated. In recent years, the concept that long non-coding RNAs (lncRNAs) contribute to protein aggregation has gained recognition. LncRNAs influence the formation of protein aggregates by facilitating protein overexpression through the regulation of gene transcription and translation, inhibiting protein degradation via lysosomal and autophagic pathways, and targeting aberrant modifications and phase transitions of proteins. A better understanding of the relationship between lncRNAs and aberrant protein aggregation is an important step in dissecting the underlying molecular mechanisms and will contribute to the discovery of new therapeutic targets and strategies.
Modeling the survival rate in syndromes associated with frontotemporal lobar degeneration (FTLD) is essential to assess disease trajectories.
In 262 patients with FTLD, we considered plasma neurofilament light chain (NfL), glial fibrillary acidic protein, brain-derived tau, phosphorylated tau217 and amyloid beta (Aβ42/Aβ40). The FTLD Survival Score (FTLD-SS) was calculated by the β coefficients of the variables independently associated with survival rate.
Increased plasma NfL levels (p < 0.001), older age at evaluation (p = 0.002), positive family history (p = 0.04), and motor phenotypes (p < 0.001) were associated with reduced survival. The predictive validity of FTLD-SS was 0.75 (95% confidence interval, 0.59–0.91) at 1 year.
Survival rate in FTLD is shaped by intensity of neurodegeneration (using plasma NfL as proxy) together with certain clinical variables. The FTLD-SS may serve as a simple tool for survival rate estimation and for patient stratification in clinical trials.
Alzheimer's disease-related biomarkers detect pathology years before symptoms emerge, when disease-modifying therapies might be most beneficial. Remote cognitive testing provides a means of assessing early cognitive changes. We explored the relationship between neurodegenerative biomarkers and cognition in cognitively normal individuals.
We remotely deployed 13 computerized Cognitron tasks in 255 Insight 46 participants. We generated amyloid load and positivity, white matter hyperintensity volume (WMHV), whole brain and hippocampal volumes at age 73, plus rates of change over 2 years. We examined the relationship between Cognitron, biomarkers, and standard neuropsychological tests.
Slower response time on a delayed recognition task predicted amyloid positivity (odds ratio [OR] = 1.79, confidence interval [CI]: 1.15, 2.95), and WMHV (1.23, CI: 1.00, 1.56). Brain and hippocampal atrophy rates correlated with poorer visuospatial performance (b = -0.42, CI: -0.80, -0.05) and accuracy on immediate recognition (b = -0.01, CI: -0.012, -0.001), respectively. Standard tests correlated with Cognitron composites (rho = 0.50, p < 0.001).
Remote computerized testing correlates with standard supervised assessments and holds potential for studying early cognitive changes associated with neurodegeneration.
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