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Insulin May Protect Against Alzheimer's
In lab study, diabetes treatments are found to slow damage

TUESDAY, Feb. 3 (HealthDay News) -- Insulin may slow or prevent the memory loss caused by Alzheimer's disease, a new study says.

Laboratory research led by a team from Northwestern University found that insulin acts as a shield that deflects the toxic proteins that attack the wiring in the brain responsible for forming memories.

"Therapeutics designed to increase insulin sensitivity in the brain could provide new avenues for treating Alzheimer's disease," William L. Klein, a researcher in Northwestern's Cognitive Neurology and Alzheimer's Disease Center and senior author of the study, said in a news release issued by the school. "Sensitivity to insulin can decline with aging, which presents a novel risk factor for Alzheimer's disease. Our results demonstrate that bolstering insulin signaling can protect neurons from harm."

The findings also add to recent evidence that has some researchers considering Alzheimer's a form of diabetes. The report was published online Feb. 2 in Proceedings of the National Academy of Sciences.

In the study, insulin and rosiglitazone (Avandia)-- an insulin-sensitizing drug used to treat type 2 diabetes -- offered protection to neurons taken from the hippocampus, one of the brain's crucial memory centers. It protected the neurons from amyloid beta-derived diffusible ligands, or ADDLs, which are proteins that are known to attach to and block memory-forming synapses, leading to memory loss.

ADDLs have been found to have a role in Alzheimer's.

"The discovery that anti-diabetic drugs shield synapses against ADDLs offers new hope for fighting memory loss in Alzheimer's disease," lead author Fernanda G. De Felice, a former visiting scientist in Klein's lab and an associate professor at the Federal University of Rio de Janeiro, Brazil, said in the same news release.

The researchers had recently found, in related work, that ADDL caused insulin resistance in the neurons it binds to by stripping the insulin receptors.

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