title: Metabolic and Non-Cognitive Manifestations of Alzheimer's Disease: The Hypothalamus as Both Culprit and Target of Pathology.
abstract: Alzheimer's disease (AD) is increasingly recognized as a complex neurodegenerative disease beginning decades prior to the cognitive decline. While cognitive deficits remain the cardinal manifestation of AD, metabolic and non-cognitive abnormalities, such as alterations in body weight and neuroendocrine functions, are also present, often preceding the cognitive decline. Furthermore, hypothalamic dysfunction can also be a driver of AD pathology. Here we offer a brief appraisal of hypothalamic dysfunction in AD and provide insight into an underappreciated dual role of the hypothalamus as both a culprit and target of AD pathology, as well as into new opportunities for therapeutic interventions and biomarker development.
authors.affiliation: Feil Family Brain and Mind Research Institute, Joan and Sanford I. Weill Medical College of Cornell University, New York, NY 10065, USA. Electronic address: mishii@med.cornell.edu.
authors.forename: Makoto
authors.initials: M
authors.lastname: Ishii
authors.affiliation: Feil Family Brain and Mind Research Institute, Joan and Sanford I. Weill Medical College of Cornell University, New York, NY 10065, USA.
authors.forename: Costantino
authors.initials: C
authors.lastname: Iadecola
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism*; D001835:Body Weight; D003071:Cognition; D004195:Disease Models, Animal; D006801:Humans; D007031:Hypothalamus / Q000378:metabolism / Q000473:pathology; D055099:Neuroendocrine Cells / Q000378:metabolism* / Q000473:pathology
chemical_list: D016229:Amyloid beta-Peptides; D015415:Biomarkers