A low dose of insulin to suppress freedom of expression in the blood of four of the precursors of proteins involved in the pathogenesis of Alzheimer's disease, according to new clinical research by the University at Buffalo endocrinologists. The research, published in March in line, in the journal of clinical endocrinology and metabolism suggests that insulin could have a powerful, new role in the fight against the disease of Alzheimer.
"Our results clearly demonstrate that insulin has the potential to develop as a therapeutic agent for Alzheimer's disease, which is not currently available, as satisfactory treatment", explains UB doctor Paresh Dandona, MD, PhD, distinguished professor of medicine at the school of medicine and biomedical sciences and lead author of the study.
One of the four proteins that is shown in the study suppressed by insulin is a precursor of beta-amyloid, the main component of plates considered the hallmark of Alzheimer's disease.
The results show for the first time that studied four precursor proteins are expressed in peripheral mononuclear cells, white blood cells are an important component of the immune system.
The document is based on the UB researchers previous work shows that insulin has a rapid and potent anti-inflammatory effect of mononuclear of peripheral cells. Also based on the association between obesity, diabetes type 2 and chronic inflammation of low quality, so that the resistance to insulin, all conditions that manifested a prevalence significantly more high of Alzheimer's disease.
In the study, 10 obese patients with type 2 diabetes had an infusion with two units of 100 ml of insulin per hour over a period of four hours. Patients taking oral drugs to treat diabetes; None of them were taking insulin or any antioxidant or anti-inflammatory nonsteroidal. The control group received dextrose 5% normal saline solution per hour.
Insulin low dose was found to suppress the expression of amyloid precursor protein, which is derived from beta-amyloid. It has also removed the presenilin-1 and presenilin-2, the two subunits of the enzyme that converts the amyloid-beta precursor protein to form amyloid plaques. Insulin also removed synthase kinase of glycogen, which phosphorylates, or in another phosphate group is added to a Neuronal protein, tau, to form tangles tangles, the other major component of Alzheimer's disease in the brain.
"Our data show, for the first time that the key peripheral mononuclear cells express some of the proteins involved in the pathogenesis of Alzheimer's disease", explains Dandona. "They show that these key cells can be used to study the effect of potential treatments for Alzheimer's disease in proteins involved in disease."
"Even more importantly, it is unlikely that insulin has a direct effect of cells in these precursors and also anti-inflammatory proteins exercising their other actions" he continues. "In this effect of insulin, and systemic studies, then insulin may be a potential therapeutic agent in the treatment of Alzheimer's disease." "The challenge is to deliver insulin directly in the brain, thus avoiding its hypoglycemic effect.".
Fortunately, said Dandona, demonstrated a preliminary inquiry earlier study delivered intranasal insulin can lead to its entry in the brain along the olfactory nerves and his administration can improve cognitive function in patients with Alzheimer's disease. However, warns that the mode of action is unknown.
"Our study provides a potential rational mechanism," he said.
Additional contributors to the study, while in the laboratory of Dandona, are Mohamed Islam; Husam Ghanim, Ph.d., Professor Assistant in medicine; Chang Ling Sia; Sandeep Dhindsa, Assistant Professor of medicine; Sonny Dandona; Antoine Makdissi, Assistant Professor of medicine; and Ajay Chaudhuri, MD, Professor of medicine.
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