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Disrupting a connection between the body’s intrinsic clock and the brain might assist in diminishing neurodegeneration in mouse models of Alzheimer’s disease, as indicated by a recent investigation led by scholars at WashU Medicine and featured in Nature Aging.

Erik Musiek, MD, PhD, the Charlotte & Paul Hagemann Professor of Neurology at WashU Medicine, alongside primary author Jiyeon Lee, PhD, and their team, examined mouse models of Alzheimer’s disease and discovered that impairing the role of a crucial protein within the circadian framework can lower the levels of a detrimental protein known as tau and mitigate neurodegeneration.

A circadian clock protein referred to as REV-ERBα is recognized for regulating daily rhythms related to metabolism and inflammation. Although it has not been extensively researched in the brain, REV-ERBα in other bodily tissues has been observed to influence nicotinamide adenine dinucleotide (NAD⁺), which is essential for cellular processes such as DNA repair and metabolism. The levels of NAD⁺ correlate directly with brain aging and neurodegeneration—lower levels equate to accelerated brain aging. Indeed, many commercially available supplements purport to elevate NAD⁺ levels to combat aging.

Musiek and his associates genetically eliminated REV-ERBα across all tissues in one cohort of mice, while in another group, the deletion occurred solely in astrocytes—glial cells that constitute a significant part of the central nervous system. In both scenarios, NAD⁺ levels rose. This demonstrated that the removal of REV-ERBα in astrocytes directly influences NAD⁺ levels within the brain, opening a pathway for prospective studies on neurodegenerative treatments in the future.

The researchers further identified that suppressing REV-ERBα, both genetically and through a new drug that has shown potential in amyloid-β pathology and Parkinson’s disease investigations, resulted in increased NAD⁺ levels and shielded the mice from tau pathology, which involves the harmful aggregation of proteins in the brain that contribute to neurodegenerative disorders. Findings from the experimental drug could pave the way for innovative therapeutic strategies to prevent and tackle Alzheimer’s disease.

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