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Could blocking a protein reduce the symptoms and progression of Alzheimer’s?
Georgios Pampalakis, Ph.D.
Aristotle University of Thessaloniki
Thessaloniki, Greece
Background
The beta-amyloid protein accumulates to form plaques in the brain, a hallmark brain change observed in Alzheimer’s. A protein called KLK6 breaks down certain other proteins inside cells, including the amyloid precursor protein, the parent protein of beta-amyloid. Previous studies have shown that levels of KLK6 may be increased in the cerebrospinal fluid (biological fluid surrounding the brain and spinal cord) of individuals with Alzheimer’s. Studies also show that KLK6, and a similarly-shaped protein called KLK8 may be associated with the accumulation of beta-amyloid. Other findings using genetically engineered Alzheimer’s-like mice have shown that blocking KLK8 may reduce brain changes observed in Alzheimer’s.
In preliminary studies, Dr. Georgios Pampalakis and colleagues found that mice without KLK6 may have lower levels of KLK8. Based on these findings and other studies, Dr. Pampalakis believes that blocking KLK6 may impact brain changes observed in Alzheimer’s and may slow disease progression.
Research Plan
Building on their preliminary findings, Dr. Pampalakis’ team will develop genetically engineered Alzheimer’s-like mice that lack KLK6. Using this mouse model, the researchers will study behavioral changes including movement and cognition. They will also study the impact of lack of KLK6 (and thereby a possible reduction in the levels of KLK8) on brain changes including levels of beta-amyloid and tau in the mice brain; the protein tau accumulates to form tangles in the brain, another hallmark brain change observed in Alzheimer’s.
Dr. Pampalakis and colleagues will also develop potential chemical compounds to block KLK6. Dr. Pampalakis believes these experiments may help in understanding the biological mechanisms by which KLK6 may be associated with the development and progression of Alzheimer’s.
Impact
The study results may help understand whether blocking or reducing the levels of KLK6 may prevent or delay the progression of Alzheimer’s. If successful, KLK6 could be a potential therapeutic target in Alzheimer’s.
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