Brain protein shows further Alzheimer's ties, could reverse symptoms

a black and white drawing of a human brain

The origins of Alzheimer’s disease have long presented researchers with a stark challenge. And researchers at the Biodesign Neurodegenerative Disease Research Center at Arizona State University have taken another step forward in discovering what may cause the disease and how to treat it.

In an article published in the journal Molecular Psychiatry, Salvatore Oddo has shed light on the protein p62, which is often associated with the neurological symptoms of Alzheimer’s. The tau protein is known to build up in the brain and destroy the network therein. But Oddo and his team have found more.

According to the new study, p62 has been demonstrated to actually regulate the buildup of amyloid beta in the brain. The plaques are thought to be a key damaging factor in the brain.

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So p62 appears now to play a central role in the disease, and increasing its levels could help prevent or reverse its symptoms, the researchers say.

In a mouse study, when animals had their expression of p62 restored, they showed significant cognitive improvements. And this is directly tied to p62’s effect on amyloid beta plaques. Effectively, p62 acts like the brain cells’ trash compactor, binding to tau tangles and marking them for degradation.

Oddo said: "These exciting finding suggest that compounds aimed at increasing p62 may have beneficial effects for Alzheimer's disease.”

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