title: Metabolic-cognitive syndrome: a cross-talk between metabolic syndrome and Alzheimer's disease.
abstract: A growing body of epidemiological evidence suggested that metabolic syndrome (MetS) and Mets components (impaired glucose tolerance, abdominal or central obesity, hypertension, hypertriglyceridemia, and reduced high-density lipoprotein cholesterol) may be important in the development of age-related cognitive decline (ARCD), mild cognitive impairment (MCI), vascular dementia, and Alzheimer's disease (AD). These suggestions proposed in these patients the presence of a "metabolic-cognitive syndrome", i.e. a MetS plus cognitive impairment of degenerative or vascular origin. This could represent a pathophysiological model in which to study in depth the mechanisms linking MetS and MetS components with dementia, particularly AD, and predementia syndromes (ARCD or MCI), suggesting a possible integrating view of the MetS components and their influence on cognitive decline. In the present article, we discussed the role of these factors in the development of cognitive decline and dementia, including underlying mechanisms, supporting their influence on β-amyloid peptide metabolism and tau protein hyperphosphorylation, the principal neuropathological hallmarks of AD. In the next future, trials could then be undertaken to determine if modifications of these MetS components including inflammation, another factor probably related to MetS, could lower risk of developing cognitive decline. Future research aimed at identifying mechanisms that underlie comorbid associations of MetS components will not only provide important insights into the causes and interdependencies of predementia and dementia syndromes, but will also inspire novel strategies for treating and preventing cognitive disorders.
authors.affiliation: Department of Geriatrics, Center for Aging Brain, Memory Unit, University of Bari, Policlinico, Piazza Giulio Cesare, 11, 70124, Bari, Italy. vfrisardi@yahoo.com
authors.forename: Vincenza
authors.initials: V
authors.lastname: Frisardi
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Solfrizzi
authors.forename: Davide
authors.initials: D
authors.lastname: Seripa
authors.forename: Cristiano
authors.initials: C
authors.lastname: Capurso
authors.forename: Andrea
authors.initials: A
authors.lastname: Santamato
authors.forename: Daniele
authors.initials: D
authors.lastname: Sancarlo
authors.forename: Gianluigi
authors.initials: G
authors.lastname: Vendemiale
authors.forename: Alberto
authors.initials: A
authors.lastname: Pilotto
authors.forename: Francesco
authors.initials: F
authors.lastname: Panza
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000502:physiology / Q000523:psychology; D000544:Alzheimer Disease / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood / Q000592:standards; D015897:Comorbidity; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D015987:Effect Modifier, Epidemiologic; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D006973:Hypertension / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D008019:Life Style; D024821:Metabolic Syndrome / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D051379:Mice; D056128:Obesity, Abdominal / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D011157:Population Dynamics; D012307:Risk Factors; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D015415:Biomarkers; D008076:Cholesterol, HDL; D016875:tau Proteins