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Researchers at VIB and KU Leuven have discovered that hibernation triggers changes in brain cells that partially resemble those in Alzheimer’s disease. Studying golden hamsters, the team identified changes in gene expression across the hibernation cycle, which resemble those associated with the accumulation of amyloid plaques in Alzheimer’s.

The findings, published in Science Advances, suggest that some early cellular changes associated with Alzheimer’s may also occur as part of a natural adaptive response, offering new ways to study the disease for therapy development.

Alzheimer’s disease affects millions of people worldwide and is characterized by the buildup of amyloid-β plaques and tangled tau proteins in the brain. These tangles contain abnormally phosphorylated tau—a form of the protein carrying excessive phosphate groups.

A gene responsible for compacting trash inside the brain appears to be a key player in Alzheimer’s disease. Doctors may be able to target it to better treat or help prevent the devastating condition, new research suggests.

John Lukens, PhD, and his research team investigated the function of the CASS4 gene after numerous studies identified it as an Alzheimer’s risk factor. They found that it helps direct brain-cleaning immune cells called microglia.

When the gene’s proper function was disrupted, the effects were dire: The microglia could no longer effectively respond to harmful plaques forming in the brain, and they were far less able to contain and compact the toxins that make up those plaques. That allowed the plaques to grow more quickly and spread more aggressively.

Read more about the research.

Researchers John Lukens, PhD, and Addie Walsh investigated the function of the CASS4 gene after it was identified as an Alzheimer’s risk factor. They found that it helps direct brain-cleaning immune cells called microglia; when the gene’s proper function was disrupted, the effects were dire.