Affiliation:
1. Department of Pharmacology and Nutritional Sciences The University of Kentucky Lexington KY 40506 USA
2. The Research Center for Healthy Metabolism The University of Kentucky Lexington KY 40506 USA
3. Division of Endocrinology Metabolism, and Nutrition Department of Medicine Claude D. Pepper Older Americans Independence Center and Duke Molecular Physiology Institute Duke University School of Medicine Durham NC 27710 USA
4. Department of Neurology The University of Kentucky Lexington KY 40506 USA
Abstract
AbstractType‐2 diabetes raises the risk for Alzheimer's disease (AD)‐type dementia and the conversion from mild cognitive impairment to dementia, yet mechanisms connecting type‐2 diabetes to AD remain largely unknown. Amylin, a pancreatic β‐cell hormone co‐secreted with insulin, participates in the central regulation of satiation, but also forms pancreatic amyloid in persons with type‐2 diabetes and synergistically interacts with brain amyloid β (Aβ) pathology, in both sporadic and familial Alzheimer's disease (AD). Growing evidence from studies of tumor growth, together with early observations in skeletal muscle, indicates amylin as a potential trigger of cellular metabolic reprogramming. Because the blood, cerebrospinal fluid, and brain parenchyma in humans with AD have increased concentrations of amylin, amylin‐mediated pathological processes in the brain may involve neuronal metabolic remodeling. This review summarizes recent progress in understanding the link between prediabetic hypersecretion of amylin and risk of neuronal metabolic remodeling and AD and suggests nutritional and medical effects of food constituents that might prevent and/or ameliorate amylin‐mediated neuronal metabolic remodeling.
Funder
National Institute on Aging
National Institute of Neurological Disorders and Stroke
Subject
Food Science,Biotechnology