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Mice Study Suggests Chronic Inflammation Triggers Alzheimer’s

Mice Study Suggests Chronic Inflammation Triggers Alzheimer's With the growing numbers of older adults, many scientists are fearful that an epidemic of Alzheimer’s will accompany societies graying.

In preparation for the aging tsunami, various teams of researchers worldwide are feverishly investigating precisely how Alzheimer’s develops.

A team of scientists under the guidance of the University of Bonn and University of Massachusetts have discovered a new signaling pathway in mice associated with the death of brain nerve cells from chronic inflammation.

The results are now being published in the scientific journal Nature.

Alzheimer’s disease gradually leads to the destruction of nerve cells and thus to significant losses in memory formation and recall.

“Many years before the initial symptoms occur, so-called plaques, which consist of incorrectly folded beta-amyloid peptides, form in the brain of affected persons,” said lead author Dr. Michael T. Heneka. In addition, there are abnormal tau protein deposits in the brain cells of the patients.

“As a result of a signal cascade, there is a chronic inflammatory reaction and the progressive loss of nerve cells,” said Dr. Eicke Latz.

Scientists from the University of Bonn and colleagues have discovered a new signaling pathway which is involved in the development of chronic inflammation of the brain cells.

Caspase-1 plays a key role and it is jointly responsible for the activation of the inflammatory reaction. The researchers detected substantially increased amounts of caspase-1 in the brains of Alzheimer’s patients in comparison to healthy persons.

These increased levels were associated with chronic inflammatory reactions of the immune cells in the brain. The scientists also observed these findings in genetically modified mice who represent a well established model of Alzheimer’s disease.

Another factor noted by researcher is the influence of gene NLRP3 – an important factor involved in the inflammatory signaling pathways which lead to the degneration and loss of brain cells.

The scientists therefore deactivated the NLRP3 gene as well as caspase-1 in the Alzheimer’s mice. As a result, there was no inflammation in the brains of these animals and they did not develop any memory loss.

In addition, there was shown to be far less beta-amyloid peptide deposited in the brain cells of the genetically silent mice. It is evident that the non-inflamed cells were able to dispose of the deposited plaques much better as “metabolic waste.”

These results indicate a starting point which may one day aid in the development of new forms of therapy for the treatment of early-stage Alzheimer’s disease.

“We are still in the basic research stage and thus therapeutic success cannot be foreseen at this time point ,” said Heneka. “There is still a long way to go until the first clinical studies.”

Source: University of Bonn

Mice Study Suggests Chronic Inflammation Triggers Alzheimer’s

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. (2018). Mice Study Suggests Chronic Inflammation Triggers Alzheimer’s. Psych Central. Retrieved on October 30, 2020, from
Scientifically Reviewed
Last updated: 8 Aug 2018 (Originally: 20 Dec 2012)
Last reviewed: By a member of our scientific advisory board on 8 Aug 2018
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