title: The therapeutic potential of metabolic hormones in the treatment of age-related cognitive decline and Alzheimer's disease.
abstract: Aging leads to a number of physiological alterations, specifically changes in circulating hormone levels, increases in fat deposition, decreases in metabolism, changes in inflammatory responses, and reductions in growth factors. These progressive changes in physiology and metabolism are exacerbated by modern culture and Western diet and give rise to diseases such as obesity, metabolic syndrome, and type 2 (non-insulin-dependent) diabetes (T2D). These age and lifestyle-related metabolic diseases are often accompanied by insulin and leptin resistance, as well as aberrant amylin production and signaling. Many of these alterations in hormone production and signaling are directly influenced by an increase in both oxidative stress and inflammation. Importantly, changes in hormone production and signaling have direct effects on brain function and the development of age-related neurologic disorders. Therefore, this review aims to present evidence on the effects that diet and metabolic disease have on age-related cognitive decline and the development of cognitive diseases, particularly Alzheimer disease. This review will focus on the metabolic hormones insulin, leptin, and amylin and their role in cognitive decline, as well as the therapeutic potential of these hormones in treating cognitive disease. Future investigations targeting the long-term effects of insulin and leptin treatment may reveal evidence to reduce risk of cognitive decline and Alzheimer disease.
authors.affiliation: School of Biomedical Sciences, Kent State University, Kent, OH, USA.
authors.forename: John
authors.initials: J
authors.lastname: Grizzanti
authors.affiliation: Department of Biology, University of Texas, San Antonio, TX, USA.
authors.forename: Hyoung-Gon
authors.initials: HG
authors.lastname: Lee
authors.affiliation: Department of Pharmacology and Therapeutic Chemistry, Universitat de Barcelona, Barcelona, Spain.
authors.forename: Antoni
authors.initials: A
authors.lastname: Camins
authors.affiliation: Department of Pharmacology and Therapeutic Chemistry, Universitat de Barcelona, Barcelona, Spain.
authors.forename: Merce
authors.initials: M
authors.lastname: Pallas
authors.affiliation: School of Biomedical Sciences, Kent State University, Kent, OH, USA; Department of Biological Sciences, Kent State University, Kent, OH, USA. Electronic address: Gcasades@kent.edu.
authors.forename: Gemma
authors.initials: G
authors.lastname: Casadesus
mesh_terms: D000375:Aging / Q000378:metabolism; D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism; D003071:Cognition; D060825:Cognitive Dysfunction / Q000188:drug therapy* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000378:metabolism / Q000627:therapeutic use*; D058228:Islet Amyloid Polypeptide / Q000378:metabolism / Q000627:therapeutic use*; D020738:Leptin / Q000378:metabolism / Q000627:therapeutic use*; D009765:Obesity / Q000378:metabolism*
chemical_list: D007328:Insulin; D058228:Islet Amyloid Polypeptide; D020738:Leptin
keywords: Alzheimer disease; Amylin; Diabetes; Insulin; Leptin; Obesity