People with early Alzheimer’s disease and related cognitive impairment who are treated with the drug donepezil can maintain mitochondrial function in their muscles, researchers report.
Mitochondria are structures inside the cells that produce energy. People with Alzheimer’s disease have been shown to have skeletal muscle mitochondrial dysfunction that begins very early in the disease process. In a new study, investigators sought to track the function of these structures in the muscles of people with early-stage Alzheimer’s disease by measuring participants’ exercise capacity and the expression of associated genes.
The results showed that participants treated with donepezil starting at least one month before exercise capacity tests appeared to have normal mitochondrial function when compared with their untreated peers with cognitive impairment. Measurements from the untreated participants revealed decline in function, as expected.
Donepezil also was found to change the expression of genes in the treated group. These included genes involved in mitochondrial regulation and function, fatty acid metabolism and muscle protein synthesis, the researchers reported.
“These results provide further evidence that skeletal muscle mitochondrial changes occur in the very early stages of Alzheimer’s disease, but are likely influenced by a common AD medicine,” wrote Jill K. Morris, Ph.D., of the University of Kansas Alzheimer’s Disease Center.
“Donepezil significantly reduces the rate of cognitive decline in early [Alzheimer’s disease], and our results suggest it may also mediate protection against reductions in skeletal muscle respiratory capacity,” she wrote.
The study is the first of its kind to directly measure muscle mitochondrial function in patients with Alzheimer’s disease, the investigators said.
Full findings were published in the journal Function.
