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Potential New Treatment Approach for Alzheimer’s

Alzheimer’s Treatment With Antibodies Shows Promise in Clearing Plaques, Aiding Cognition

New research suggests a different therapeutic approach may be helpful in reducing the effects of Alzheimer’s disease. In the study, University of Kentucky investigators discovered an antibody that targets neuro-inflammation may reduce the development of amyloid plaques and neurofibrillary tangles and improve cognition.

Alzheimer’s disease affects more than 3 million Americans each year. Most people with Alzheimer’s develop what is called the late-onset variety in which symptoms first appear in their mid-60s. However, early-onset Alzheimer’s can begin with symptoms between a person’s 30s and mid-60s.

The first symptoms of Alzheimer’s vary from person to person. Dementia is the term applied to a group of symptoms that negatively impact memory, but Alzheimer’s is a progressive disease of the brain that slowly causes impairment in memory and cognitive function.

The new findings and approach result from an explosion of genetic data suggesting the risk for sporadic Alzheimer’s disease is driven by a variety of factors including neuroinflammation, membrane turnover and storage, and lipid metabolism.

Investigators said current therapeutic approaches for Alzheimer’s focus on the major pathological hallmarks of the disease, the plaques and tangles. Indeed, these factors are the pathological requirements for a diagnosis of Alzheimer’s.

In this study, published in the Journal of Neuroinflammation, scientists focused on triggering a receptor expressed on myeloid cell-2 (TREM2) to reduce or prevent the development of the amyloid plaques and neurofibrillary tangles. They believe creating an antibody could activate the cell receptor an opposite action that occurs when a mutation suppress the cell resulting in Alzheimer’s.

“TREM2 was identified several years ago as a gene that, when there’s a mutation, significantly increases risk of Alzheimer’s disease. The field thinks that this mutation reduces the function of the receptor, so we hypothesized that targeting TREM2 to increase its function might be a valid treatment for Alzheimer’s,” explained Dr. Donna Wilcock, associate director of the University of Kentucky’s Sanders-Brown Center on Aging (SBCoA).

Researchers found that the therapeutic targeting of TREM2 using a TREM2-activating antibody leads to the activation of microglia, recruitment of microglia to amyloid plaques, reduced amyloid deposition, and ultimately improved cognition.

“The big takeaway is that this is the first approach that targets TREM2 to promote microglia to clear the amyloid deposits in the brain that are thought to be the cause of Alzheimer’s,” said Wilcock.

The biopharmaceutical company Alector developed the antibody for this study which was conducted on mice. Due to the study’s success, SBCoA is set to be a site for an upcoming clinical trial using this new approach.

Source: University of Kentucky/EurekAlert

Alzheimer’s Treatment With Antibodies Shows Promise in Clearing Plaques, Aiding Cognition

Rick Nauert PhD

Rick Nauert, PhDDr. Rick Nauert has over 25 years experience in clinical, administrative and academic healthcare. He is currently an associate professor for Rocky Mountain University of Health Professionals doctoral program in health promotion and wellness. Dr. Nauert began his career as a clinical physical therapist and served as a regional manager for a publicly traded multidisciplinary rehabilitation agency for 12 years. He has masters degrees in health-fitness management and healthcare administration and a doctoral degree from The University of Texas at Austin focused on health care informatics, health administration, health education and health policy. His research efforts included the area of telehealth with a specialty in disease management.

APA Reference
Nauert PhD, R. (2020). Alzheimer’s Treatment With Antibodies Shows Promise in Clearing Plaques, Aiding Cognition. Psych Central. Retrieved on November 26, 2020, from
Scientifically Reviewed
Last updated: 31 Aug 2020 (Originally: 31 Aug 2020)
Last reviewed: By a member of our scientific advisory board on 31 Aug 2020
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