Washington: A new clinical research by University at Buffalo endocrinologists has shown that a low dose of insulin can suppress the expression in the blood of four precursor proteins involved in the pathogenesis of Alzheimer`s disease.
The research suggests that insulin could have a powerful, new role to play in fighting Alzheimer`s disease.
"Our results show clearly that insulin has the potential to be developed as a therapeutic agent for Alzheimer`s, for which no satisfactory treatment is currently available," said Paresh Dandona, UB distinguished professor of medicine in the School of Medicine and Biomedical Sciences and senior author on the study.
In the study, 10 obese, type 2 diabetic patients were infused with two 100 ml units of insulin per hour over a period of four hours. The patients were all taking oral drugs to treat their diabetes; none of them were taking insulin or any antioxidant or nonsteroidal anti-inflammatory drugs. The control group received 5 percent dextrose per hour or normal saline solution.
The low-dose insulin was found to suppress the expression of amyloid precursor protein, from which beta amyloid is derived. It also suppressed presenilin-1 and presenilin-2, the two subunits of an enzyme that converts amyloid precursor protein into beta amyloid, which forms the amyloid plaques. Insulin also suppressed glycogen synthase kinase, which phosphorylates, or adds on another phosphate group, to another neuronal protein, tau, to form the neurofibrillary tangles, the other important component of Alzheimer`s disease in the brain.
"Our data show, for the first time, that the peripheral mononuclear cells express some of the key proteins involved in the pathogenesis of Alzheimer`s disease," said Dandona.
"They demonstrate that these cells can be used for investigating the effect of potential Alzheimer`s disease therapies on key proteins involved in the disease.
"Even more importantly, it is likely that insulin has a direct cellular effect on these precursor proteins while also exerting its other anti-inflammatory actions," he continued.
"If this effect of insulin proves, in larger studies, to be systemic, then insulin may well be a potential therapeutic agent in treating Alzheimer`s disease. The challenge is to deliver insulin directly into the brain, thus avoiding its hypoglycemic effect," he added.
The study has been published in the Journal of Clinical Endocrinology and Metabolism.
ANI
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