According to a study published in the Journal of Experimental Medicine, scientists at the University of Southern California discovered that a drug used for the treatment of stroke may also prevent Alzheimer's disease. The study shows that the brains of Alzheimer-model mice were protected from Alzheimer-like symptoms by a genetically modified version of a human blood protein (activated protein C) called ‘3K3A-APC’. The drug specifically protected the brain by reducing the buildup of toxic amyloid-beta peptides, preventing memory loss, and reducing inflammation—all common features of Alzheimer disease.
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3K3A-APC also reduces inflammation and protects both neurons and the cells that line the walls of blood vessels. Besides treating stroke--the protein was also shown to have positive effects on other models of disease including traumatic brain injury (TBI) and multiple sclerosis, and was clinically proven to be safe well-tolerated and capable of reducing intracerebral bleeding. "Because of its neuroprotective, vasculoprotective, and anti-inflammatory activities in multiple models of neurological disorders, we investigated whether 3K3A-APC can also protect the brain from the toxic effects of amyloid-beta toxin in a mouse model of Alzheimer's disease," says Berislav V. Zlokovic, the Director of the Zilkha Neurogenetic Institute at the Keck School of Medicine, University of Southern California.
3K3A-APC (right) greatly reduced the amount of amyloid-beta (green) that accumulated in brains of model mice that develop Alzheimer like symptoms in comparison with no treatment (left).
Credit: Lazic et al., 2019 via Science Daily
In the paper, 3K3A-APC protected the brain by preventing nerve cells from synthesizing an enzyme called BACE1 that in return produces amyloid-beta. Although several different inhibitors of BACE1 have gone through clinical trials, using 3K3A-APC for the inhibition of BACE1 is an alternative approach especially at early stages of the Alzheimer when amyloid-beta has not yet to accumulated to dangerous levels resulting in permanent damage in the brain. "Our present data support the idea that 3K3A-APC holds potential as an effective anti-amyloid-beta therapy for early stage Alzheimer's disease in humans," Zlokovic says.
Source: Science Daily
