Providence, RI By depleting insulin and its related proteins in the brain, researchers at Rhode Island Hospital and Brown Medical School have replicated the progression of Alzheimer's disease including plaque deposits, neurofibrillary tangles, impaired cognitive functioning, cell loss and overall brain deterioration in an experimental animal model. The study demonstrates that Alzheimer's is a brain-specific neuroendocrine disorder, distinct from other types of diabetes.
In the study, brain deterioration was not related to the pancreas, which regulates insulin for the body. When pancreatic insulin is deficient or the body fails to respond to it, the result is Type 1 or Type 2 diabetes. Previous work by the researchers with postmortem brain tissue of Alzheimer's patients showed a strong link between insulin depletion in the brain and Alzheimer's disease, raising the possibility that Alzheimer's is a neuroendocrine disorder, or a Type 3 diabetes.
"We have demonstrated that a loss of insulin in the brain triggers the onset of Alzheimer's, probably because as the brain loses insulin, the cells that require insulin to function and survive also eventually die. The consequences are increased oxidative stress, brain deterioration, loss of cognitive function, and a buildup of plaques and tangles in the brain all hallmarks of Alzheimer's, says senior author Suzanne M. de la Monte, MD, MPH, a neuropathologist at Rhode Island Hospital and a professor of pathology and clinical neuroscience at Brown Medical School in Providence, RI.
"We now know that if you specifically target insulin and its actions in the brain, you could develop new treatments for this disease," de la Monte says.
The study is published in the current issue (Volume 9, Issue 1) of the Journal of Alzheimer's Disease (http://www.j-alz.com).
Researchers injected the brains of rats with Streptozotocin (STZ), a compound that when metaboliPage: 1 2 3 Related medicine news :1
Contact: Nicole Gustin
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