Mutations associated with hereditary Alzheimer's disease may disrupt signal transmission from nerves to muscles independently of brain damage. This was demonstrated in experiments conducted by researchers at the University of Central Florida and Hesperos. The study was published in Alzheimer's & Dementia in April 2026.
People with Alzheimer's disease sometimes experience difficulties with walking, balance and coordination. These problems are usually considered in the context of changes in the central nervous system. The researchers set out to investigate whether impaired nerve-muscle communication could develop directly as a result of disease-associated mutations.
To do this, they created a neuromuscular junction-on-a-chip. The system combined healthy human muscle cells with motor neurons derived from stem cells carrying mutations associated with familial Alzheimer's disease. The model did not include the brain or spinal cord.
The researchers assessed how reliably nerve signals triggered muscle contractions and how quickly fatigue developed. Neurons carrying the mutations impaired the functioning of the neuromuscular junction even when the muscle cells were healthy.
The findings suggest that some motor problems may have an independent mechanism outside the brain. They also help explain why treatments targeting only the central nervous system may potentially fail to address all manifestations of the disease.
However, the cellular model does not establish the sequence in which symptoms appear in patients. The study focuses on a rare hereditary form of Alzheimer's disease and does not yet offer a ready-to-use test for the early diagnosis of the more common age-related form.
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