Proteasomes and
Brain Cell Death: Using mouse brains, scientists studied
the role of the
proteasome system in neurodegenerative disorders.
Karen Duff, Ph.D.,
Columbia University.
(Ddecember 21, 2015) NIH-funded
mouse study identifies therapeutic target for clearing out toxic proteins
damaged during neurodegenerative disorders.
A study of mice shows how proteasomes, a cell’s waste
disposal system, may break down during Alzheimer’s disease, creating a cycle in
which increased levels of damaged proteins become toxic, clog proteasomes, and
kill neurons. The study, published in Nature Medicine and supported by the
National Institutes of Health, suggests that enhancing proteasome activity with
drugs during the early stages of Alzheimer’s may prevent dementia and reduce
damage to the brain.
“This exciting research advances our understanding of the
role of the proteasomes in neurodegeneration and provides a potential way to
alleviate symptoms of neurodegenerative disorders,” said Roderick Corriveau,
Ph.D., program director at the NIH’s National Institute of Neurological
Disorders and Stroke (NINDS), which provided funding for the study.
The proteasome is a hollow, cylindrical structure which
chews up defective proteins into smaller, pieces that can be recycled into new
proteins needed by a cell. To understand how neurodegenerative disorders affect
proteasomes, Natura Myeku, Ph.D., a postdoctoral fellow working with Karen E.
Duff, Ph.D., professor of pathology and cell biology at Columbia University,
New York City, focused on tau, a structural protein that accumulates into
clumps called tangles in the brain cells of patients with Alzheimer’s disease
and several other neurodegenerative disorders known as tauopathies.