What is it about?
Alzheimer's disease begins with accumulation of amyloid-beta protein in the brain. But how it occurs and progresses to Alzheimer's disease remain elusive. Recent findings from a cohesinopathy mouse model (a genomic instability research model we have used for carcinogenesis studies) suggest mitosis, both its entry and prolongation, may be critical to accumulate amyloid-beta in brain and to develop Alzheimer's disease.
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Why is it important?
Currently there is no drug that can intervene and/or cure Alzheimer's disease. The findings suggest novel ways to intervene amyloid-beta accumulation.
Perspectives
This is the first study connecting mitosis/genomic instability research to a major disease other than cancer (i.e., Alzheimer's disease), expanding disease relevance of the research field. My specialty, "genomic instability in the body", has been studied in the context of cancer. Investigation of "genomic instability, aging and cancer" under a new hypothesis led to the new findings linking mitosis study to Alzheimer's disease. I am hopeful that our transgenic mouse-based study leads to elucidation of mechanism of cerebral amyloid-beta accumulation and rapid development of drugs for intervention and therapy.
Hiroshi Yamada
University of Oklahoma
Read the Original
This page is a summary of: Critical role of mitosis in spontaneous late-onset Alzheimer’s disease; from a Shugoshin 1 cohesinopathy mouse model, Cell Cycle, September 2018, Taylor & Francis,
DOI: 10.1080/15384101.2018.1515554.
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