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Scientists identify drugs that could reverse cognitive decline

American and Israeli scientists have found that drugs that quell inflammation in the brain could also slow and even reverse cognitive decline, which is associated with diseases such as dementia.

Th researchers found that mice with cognitive decline were able to learn new tasks and showed similar brain function to mice half their age when administered one such drug.

The two research papers – co-authored by academics from UC Berkeley and Ben-Gurion University – point to a new way of approaching dementia and cognitive decline, identifying inflammation of the brain and a “leaky blood-brain barrier” as potential key causes.

“We tend to think about the aged brain in the same way we think about neurodegeneration: age involves loss of function and dead cells. But our new data tell a different story about why the aged brain is not functioning well. It is because of this “fog” of inflammatory load,” said Daniela Kaufer, a UC Berkeley professor of integrative biology and co-author of the study.

“But when you remove that inflammatory fog, within days the aged brain acts like a young brain. It is a really, really optimistic finding, in terms of the capacity for plasticity that exists in the brain. We can reverse brain ageing.”

Research in the area of brain inflammation shows that as we age, the filtration system that prevents molecules or infectious organisms in the blood from leaking into the brain – the blood-brain barrier – becomes leaky, letting in chemicals that cause inflammation and cell death.

One of the papers shows that the inflammatory fog induced by a leaky blood-brain barrier alters the mouse brain’s normal rhythms, causing microseizure-like events that could produce some of the symptoms seen in degenerative brain diseases like Alzheimer’s disease.

Three of the researchers have started a company to develop a drug to heal the blood-brain barrier for clinical treatment and hope that the drug will help reduce brain inflammation after stroke, concussion or traumatic brain injury, and eventually help older adults with dementia who have demonstrated leakage of the blood-brain barrier.

“We got to this through this back door; we started with questions about plasticity having to do with the blood-brain barrier, traumatic brain injury and how epilepsy develops,” Kaufer said. “But after we’d learned a lot about the mechanisms, we started thinking that maybe in ageing it is the same story.

“This is new biology, a completely new angle on why neurological function deteriorates as the brain ages.”

The two papers were released in the journal, Science Translational Medicine

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