Clocks & Sleep Neurodegeneration/HPAN News

Sleep aid blocks neurodegeneration in mice

A new study by WashU Medicine researchers suggests that lemborexant and sleep aids that work the same way could help treat or prevent damage caused by harmful buildup of the protein tau in multiple neurodegenerative diseases, including Alzheimer’s. Shown are cross-sections of brain tissue from two mice genetically prone to tau accumulation. Treatment with lemborexant (right) results in larger volume in the hippocampus (central purple spiral), important for memory, and a smaller gap in brain tissue (white space) compared with no treatment (left). (Image: Samira Parhizkar)

A common sleep aid restores healthier sleep patterns and protects mice from the brain damage seen in neurodegenerative disorders, such as Alzheimer’s disease, according to new research from Washington University School of Medicine in St. Louis. The drug, lemborexant, prevents the harmful buildup of an abnormal form of a protein called tau in the brain, reducing the inflammatory brain damage tau is known to cause in Alzheimer’s.

The study suggests that lemborexant and other drugs that work in the same way could help treat or prevent the damage caused by tau in multiple neurodegenerative diseases, including Alzheimer’s, progressive supranuclear palsy, corticobasal syndrome and some frontotemporal dementias.

The study is published May 27 in Nature Neuroscience.

“We have known for a long time that sleep loss is a risk factor for Alzheimer’s disease,” said senior author David M. Holtzman, MD, the Barbara Burton and Reuben M. Morriss III Distinguished Professor of Neurology at WashU Medicine. “In this new study, we have shown that lemborexant improves sleep and reduces abnormal tau, which appears to be a main driver of the neurological damage that we see in Alzheimer’s and several related disorders. We are hopeful this finding will lead to further studies of this sleep medication and the development of new therapeutics that may be more effective than current options either alone or in combination with other available treatments.

“The antibodies to amyloid that we now use to treat patients with early, mild Alzheimer’s dementia are helpful, but they don’t slow the disease down as much as we would like,” he added. “We need ways to reduce the abnormal tau buildup and its accompanying inflammation, and this type of sleep aid is worth looking at further. We are interested in whether going after both amyloid and tau with a combination of therapies could be more effective at slowing or stopping the progression of this disease.”