Researchers identify link between muscle loss and cognitive decline using multimodal neuroimaging

2024-06-25     Kim Ji-hye

Korean researchers said they utilized multimodal neuroimaging to identify the origins of cognitive decline associated with muscle loss.

Sarcopenia, characterized by the loss of muscle mass, has long been associated with heightened risks among older adults, such as fractured bones from falls, decline in gait performance, and diminished daily activities. 

Muscle loss has been implicated in cognitive impairments stemming from Alzheimer's disease and vascular dementia, with cognitive impairment prevalence in sarcopenic individuals estimated between 9.9 percent to 40.4 percent among those aged 60 years or older. Older adults with sarcopenia face twice the risk of cognitive decline, according to a prior meta-analysis. 

Path model links cognitive function, sarcopenia subcomponents, and brain pathologies including atrophy, amyloid beta retention, and white matter changes. (Source: Alzheimer's & Dementia)

The exact ways in which sarcopenia influences cognitive decline, including complex cerebral changes such as retention of amyloid-beta (Aβ), alterations in brain vasculature, and reduced cortical thickness, remain elusive.

A research team, led by Professor Lim Hyun-kook at the Department of Psychiatry at the Catholic Brain Health Center, Yeouido St. Mary’s Hospital, analyzed the relationship between sarcopenia scores—measured by muscle mass, muscle strength, and physical function—and various brain metrics in 528 non-demented participants from the Catholic Aging Brain Imaging (CABI) database.

Their analysis of brain metrics included cortical thickness, hippocampal volume, white matter disease, and cerebral amyloid angiopathy (CAA) assessed using amyloid-positron emission tomography (PET) CT, alongside cognitive function.

They discovered significant correlations between muscle mass, measured by skeletal muscle index (SMI), muscle strength assessed by hand grip strength (HGS), and physical function evaluated with the five times sit-to-stand test (5STS), with cognitive impairment. Each of these factors exhibited distinct associations with brain atrophy, white matter disease, and amyloid deposition.

Statistical maps show cortical thickness and amyloid retention in sarcopenia vs. non-sarcopenia groups (A). Correlations between cortical thickness and grip strength (B), 5 times sit-to-stand (C, D), and amyloid retention with muscle mass (E–H). (Source: Alzheimer's & Dementia)

Lower muscle mass correlated with  Aβ retention, a trigger for Alzheimer's disease. Weaker muscle strength correlated with a reduction in cortical thickness in the temporal pole, while poorer muscle function was linked to greater atrophy in the insular cortex.

"Maintaining muscle volume, strength, and function in old age is crucial for preventing degenerative changes in the brain and cognitive decline,” said Dr. Kim Sung-hwan, clinical instructor at the Catholic University of Korea Seoul St. Mary's Hospital and lead author of the study.

These correlations persisted even after adjusting for variables such as age, gender, education, apolipoprotein E (APOE) genotype, and depression, using partial least squares structural equation modeling (PLS-SEM). Higher muscle mass appeared to inhibit Aβ retention, while stronger muscles appeared to provide protection against white matter disease, thereby preserving cognitive function.

Professor Lim said, "Addressing sarcopenia-related physical conditions medically could represent a novel therapeutic avenue for reducing the risk of developing dementia,” emphasizing the potential therapeutic implications.

The study results were published in Alzheimer's & Dementia, the journal of the Alzheimer's Association.

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