Stroke Medicine May Prevent Beta-Amyloid Accumulation in Early Alzheimer’s, Mouse Study Shows

Stroke Medicine May Prevent Beta-Amyloid Accumulation in Early Alzheimer’s, Mouse Study Shows
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A medicine being developed to treat stroke patients may help protect the brain from Alzheimer’s disease by suppressing the accumulation of toxic amyloid-beta during the early stages of the disease and preventing memory loss, a mouse study shows.

The study “3K3A-activated protein C blocks amyloidogenic BACE1 pathway and improves functional outcome in mice” was published in The Journal of Experimental Medicine

“Our present data support the idea that 3K3A-APC holds potential as an effective anti-amyloid-β [beta] therapy for early stage Alzheimer’s disease in humans,” Berislav V. Zlokovic, lead author of the study, said in a press release. Zlokovic is director of the Zilkha Neurogenetic Institute at the Keck School of Medicine, University of Southern California.

3K3A-APC, a genetically modified form of a natural human blood protein called activated protein C (APC), was shown to have beneficial therapeutic effects in mouse models of stroke, amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS).

The therapy reduces inflammation and protects neurons from a programmed cell death (called apoptosis). It also helps maintain the integrity of cells that line the walls of blood vessels after an injury and those of the blood brain barrier, a highly selective membrane that shields the central nervous system from the general blood circulation.

Researchers at the University of Southern California hypothesized that because 3K3A-APC has multiple benefits in several models of neurological disorders, it also could protect the brain from toxic effects of amyloid-beta deposition, a hallmark of Alzheimer’s disease.

“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-β toxin in a mouse model of Alzheimer’s disease,” Zlokovic said.

Researchers treated a mouse model of Alzheimer’s disease with daily injections of 3K3A-APC or an innocuous substance (control group), delivered intraperitoneally (directly into the abdomen) for four months.

Treatment with 3K3A-APC led to a significant reduction of total brain amyloid-beta load, by 40 to 50%, when compared to controls, specifically in two regions of the brain: the hippocampus and cortex.

The effects of 3K3A-APC in the hippocampus, linked to memory and spatial navigation, were in agreement with the therapy’s functional benefits; the treatment prevented memory loss in these animals. Additionally, 3K3A-APC helped maintain a normal cerebral blood flow and suppressed neuroinflammation, commonly seen in Alzheimer’s disease.

3K3A-APC, researchers found, works by preventing the production of the BACE1 enzyme, a key factor required for the synthesis of amyloid-beta. BACE1 is one of the prime targets of Alzheimer’s therapies seeking to reduce the levels of amyloid-beta in the brains of Alzheimer’s patients.

Increasing evidence suggests that the optimal timing for BACE1 inhibitors to be effective is during the early stages of the disease, before amyloid-beta accumulation occurs, leading to permanent brain damage.

“Since 3K3A-APC is safe and well tolerated in humans including stroke patients, the present data support that 3K3A-APC holds potential as an effective anti-Aβ [amyloid-beta] therapy for early-stage AD [Alzheimer’s disease] in humans,” researchers wrote.

This is not the first time a stroke therapy has shown potential to treat Alzheimer’s disease. In October 2018, fasudil, a chemical inhibitor used to treat strokes, also was suggested as a potential therapy for preventing early nerve cell impairment and beta-amyloids’ damaging effects.

Patricia holds a Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She has also served as a PhD student research assistant at the Department of Microbiology & Immunology, Columbia University, New York.
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Patricia holds a Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She has also served as a PhD student research assistant at the Department of Microbiology & Immunology, Columbia University, New York.
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