Dementia can be treated on an accelerated basis.
Researchers at Columbia University have found new evidence to support the “amyloid hypothesis” but have unearthed previously unknown details that allowed them to propose a new treatment approach. The article was published in Science Advances.
Scientists analyzed the brain cells of people with Alzheimer’s disease and found that its symptoms may indeed be caused by the accumulation of aggregates of beta-amyloid proteins in the brain. But scientists have found that it’s not the amyloids themselves, but the fact that they serve as “glue” for two other proteins in brain neurons – ATF4 and CREB3L2.
After pairing CREB3L2-ATF4, a network of other proteins is activated, causing the accumulation of tau protein aggregates inside neurons, which lead to the symptoms of dementia.
This protein pair also shuts down the cellular machinery that clears old and damaging proteins from neurons, another sign of Alzheimer’s disease.
The researchers found that although CREB3L2 and ATF4 are also found alone in healthy neurons, their binding together is greatly increased in the presence of excess amyloid.
Scientists have identified the drug dovitinib, which prevents the formation of the CREB3L2-ATF4 pair. Dovitinib was previously approved by the FDA for the treatment of kidney cancer, but has not been tested for the treatment of Alzheimer’s disease.
This means it might be approved for fast track dementia treatment.
The scientists added that the drug is non-toxic to neurons and penetrates the brain through the blood-brain barrier.
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