New research reveals that blood markers linked to Alzheimer’s disease signal a faster decline in muscle strength among older adults, highlighting an opportunity for early detection and preventive interventions against age-related muscle loss.
Study: Blood biomarkers of Alzheimer’s disease and 12-year muscle strength trajectories in community-dwelling older adults: a cohort study. Image credit: Toa55/Shutterstock.com
A recent Lancet Healthy Longevity study examined the relationship between Alzheimer's disease (AD) biomarkers and muscle strength.
The study suggests that early detection of Alzheimer’s disease (AD)-related biomarkers is associated with progressive muscle strength decline and could help prevent sarcopenia via quick interventions among older adults.
Sarcopenia and aging
Sarcopenia is a geriatric condition characterized by a decline in muscle strength and mass, commonly occurring with aging. Previous studies have shown that, compared to muscle mass, muscle strength is a more accurate indicator of adverse health outcomes. Therefore, understanding the underlying causes of muscle strength decline is crucial for effectively preventing sarcopenia.
In addition to age-related metabolic and structural changes in muscle, skeletal muscle performance is also influenced by several chronic diseases, including cerebrovascular diseases, diabetes, cardiovascular conditions, and respiratory diseases. An individual’s muscle performance is also linked to lifestyle factors, as well as biological and psychosocial parameters. Compared to men, women experience earlier and more prominent muscle strength decline with age.
Neurodegeneration and muscle strength decline
Reduced motor nerve performance has been associated with decreased muscular performance. Neurodegeneration is characterized by changes in neuromuscular signaling and impaired muscle fiber recruitment, both of which promote atrophy. AD patients often experience muscle deterioration, even in the preclinical stages of the disease.
Previous studies have established a link between the APOE ε4 genotype, a genetic risk factor for Alzheimer's disease (AD), and poorer motor function. Reduced muscle strength has been associated with an increased risk of AD and a faster rate of cognitive decline. Although an association between AD and sarcopenia has been established, the mechanisms behind this muscle–brain interaction remain unclear.
Understanding the longitudinal relationship between AD-related biomarkers, such as amyloid β (Aβ), phosphorylated tau (p-tau), glial fibrillary acidic protein (GFAP), total tau (t-tau), and neurofilament light chain, and muscle strength in dementia-free, community-dwelling older adults is essential.
About the study
The current research obtained data from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), an ongoing prospective study conducted in Sweden. The aim was to investigate the relationship between blood concentrations of AD biomarkers and changes in muscle strength over time in dementia-free, community-dwelling older adults.
The SNAC-K study, conducted between 2001 and 2004, included individuals aged 60 and above. Participants younger than 78 were followed up every six years, while those aged 78 and older were followed up every three years. The current study included data from baseline to the fourth follow-up. Individuals diagnosed with dementia, AD, or Parkinson's disease, as well as those residing in institutions at baseline, were excluded.
Muscle strength was assessed using the handgrip strength test and the chair-stand test. Blood samples were collected to measure AD biomarkers and determine APOE genotype. Baseline data included personal, lifestyle, and anthropometric information, such as age, sex, education, marital status, and smoking status. Notably, 99% of the study cohort consisted of White individuals.
The association between baseline levels of AD-related biomarkers and changes in muscle strength over time was assessed using linear mixed models with random intercept and slopes.
Findings
A total of 1,953 participants met the eligibility criteria. Of these, 39.9% were male and 60.1% were female, with a mean age of 70.2 years. Approximately 14.5% of males and 28.0% of females exhibited low strength in both tests. Impaired performance in the chair-stand test was observed in 25.3% of males and 35.5% of females.
Blood sample analysis revealed differences in the distributions of AD biomarkers between sexes. Participants with low muscle strength exhibited higher concentrations of neurofilament light chain, p-tau217, p-tau181, t-tau, and GFAP, as well as a lower ratio of Aβ42 to Aβ40.
Twelve-year longitudinal analyses revealed that a one-standard-deviation (SD) increase in p-tau181, p-tau217, and neurofilament light chain was associated with a more rapid decline in handgrip strength, even after adjusting for potential confounders. Similar trends were observed in associations between AD-linked biomarkers and handgrip strength.
The chair-stand test also indicated that a one-standard-deviation increase in p-tau181, p-tau217, neurofilament light chain, and GFAP correlated with a more rapid decline in muscle performance over time. Further adjustments for the time-varying Mini-Mental State Examination (MMSE) score revealed a reduction in the annual rate of decrease in lower limb strength. Similar findings were obtained in the primary model for incident dementia.
However, a contradictory finding emerged in a stratified analysis by APOE genotype. The biomarker p-tau181 was associated with a more rapid decline in chair-stand test performance. This association between AD-related biomarkers and muscle strength decline in both tests was more pronounced in younger participants and those who were physically inactive.
Conclusions
The current study established associations between AD-linked biomarkers, particularly p-tau217, tau181, neurofilament light chain, and GFAP, and muscle strength decline in older adults without dementia. It is worth noting that these associations are influenced by various factors, including age, genetic predisposition to Alzheimer’s disease, sex, and systemic inflammation.
Scientists believe that exploiting AD-related biomarkers to detect individuals at high risk of sarcopenia could enable clinicians to provide them with necessary interventions earlier.
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