Introduction: Our objective was to investigate the effect of sex on cognitive decline within the context of amyloid β (Aβ) burden and apolipoprotein E genotype.
Methods: We analyzed sex-specific effects on Aβ-positron emission tomography, apolipoprotein, and rates of change on the Preclinical Alzheimer Cognitive Composite-5 across three cohorts, such as the Alzheimer's Disease Neuroimaging Initiative, Australian Imaging, Biomarker and Lifestyle, and Harvard Aging Brain Study (n = 755; clinical dementia rating = 0; age (standard deviation) = 73.6 (6.5); female = 55%). Mixed-effects models of cognitive change by sex, Aβ-positron emission tomography, and apolipoprotein ε4 were examined with quadratic time effects over a median of 4 years of follow-up.
Results: Apolipoprotein ε4 prevalence and Aβ burden did not differ by sex. Sex did not directly influence cognitive decline. Females with higher Aβ exhibited faster decline than males. Post hoc contrasts suggested that females who were Aβ and apolipoprotein ε4 positive declined faster than their male counterparts.
Discussion: Although Aβ did not differ by sex, cognitive decline was greater in females with higher Aβ. Our findings suggest that sex may play a modifying role on risk of Alzheimer's disease-related cognitive decline.
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http://dx.doi.org/10.1016/j.jalz.2018.04.010 | DOI Listing |
Alzheimers Dement (Amst)
January 2025
Department of Neurology Massachusetts General Hospital, Harvard Medical School Boston Massachusetts USA.
Introduction: Timely detection and tracking of Alzheimer's disease (AD) -related cognitive decline has become a public health priority. We investigated whether the NIH Toolbox for Assessment of Neurological and Behavioral Function-Cognition Battery (NIHTB-CB) detects AD-related cognitive decline.
Methods: = 171 participants (age 76.
Alzheimers Dement (Amst)
January 2025
Health Care Research Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE) Greifswald Mecklenburg-Vorpommern Germany.
Introduction: This study investigated the association between modifiable factors and symptom progression in dementia over up to 8 years.
Methods: Multilevel growth curve models assessed the role of modifiable risk factors (low education, hearing impairment and its treatment, depression, physical inactivity, diabetes and its treatment, smoking, hypertension and its treatment, obesity, alcohol consumption, social isolation, and visual impairment) on cognitive and functional trajectories in 353 people with dementia.
Results: Higher education was associated with higher initial cognitive status but faster decline.
Cereb Circ Cogn Behav
December 2024
The George Institute for Global Health, Sydney, Australia.
Introduction: Cumulative blood pressure metrics may provide greater precision for measuring temporal risk exposure, especially in later life where data are mixed regarding associations of high blood pressure (BP) on cognitive function. We examined the relationship between greater cumulative exposure to high BP in later life and several domains of cognitive function.
Methods: Individual cognitive assessment scores and BP measurements in older adults (age ≥70 years) at baseline and over approximately 8 years of follow-up were available in the population-based Canadian Victoria Longitudinal Study (VLS) and Swedish Gothenburg H70 Birth Cohort Studies (H70).
Front Psychol
December 2024
Department of Neurology, Harvard Medical School, Boston, MA, United States.
Objective: This study examined the psychometric properties of a newly developed scale for measuring subjective cognitive reserve (SCR) across multiple domains, including nutrition, physical condition, sleep, cognition, willingness to learn, socialization, general health, and life plan.
Method: The relationship between SCR scores and other established measures of cognitive reserve and subjective cognitive decline was also explored. A sample of 402 healthy participants aged 18 to 79 years took part in the study.
Alzheimer's disease (AD) is the most prevalent neurodegenerative dementia, marked by progressive cognitive decline and memory impairment. Despite advances in therapeutic research, single-target-directed treatments often fall short in addressing the complex, multifactorial nature of AD. This arises from various pathological features, including amyloid-β (Aβ) aggregate deposition, metal ion dysregulation, oxidative stress, impaired neurotransmission, neuroinflammation, mitochondrial dysfunction, and neuronal cell death.
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