For the first time, using a mouse model of Alzheimer's disease, scientists have documented a link between raised levels of calcium in mitochondria and neuronal death in the living brain.
This relationship was previously documented in cell culture, but seeing this phenomenon in living mice makes it more likely that this occurs in people also and could point to a new target for Alzheimer's disease.
We were able to show mitochondrial calcium dysregulation in the neurons of living mice with Alzheimer's-like symptoms using cutting edge live imaging techniques." Maria Calvo-Rodriguez, PhD, Study Lead Author, Department of Neurology at Massachusetts General Hospital. The senior author is Brian J. Bacskai, PhD. Calvo-Rodriguez and Bacskai are both from the Department of Neurology at Massachusetts General Hospital.
Their collaborators included researchers from Harvard School of Public Health and the School of Medicine at Instituto de Investigacion Biomedica de Cadiz (INIBICA) in Spain. This study was recently published in Nature Communications .
One of the defining hallmarks of Alzheimer's disease is the deposition of amyloid beta plaques and loss of neurons. The accumulation of amyloid beta has long been thought to be a trigger of the disease, but the exact means by which neurons die in Alzheimer's remain a mystery, and the amyloid beta theory has become controversial because so many drug candidates targeting amyloid beta have failed in clinical trials.
One of the effects of amyloid beta plaques is that they cause high calcium ion (Ca2+) levels in the brain cells. There is also evidence that, at least in cell culture, exposure to amyloid beta can raise Ca2+ levels within mitochondria and lead to neuronal death. Related Stories
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