peptide-yy and Alzheimer-Disease

peptide-yy has been researched along with Alzheimer-Disease* in 2 studies

Reviews

1 review(s) available for peptide-yy and Alzheimer-Disease

ArticleYear
Neuropeptide Y, peptide YY and aluminum in Alzheimer's disease: is there an etiological relationship?
    Journal of inorganic biochemistry, 2001, Volume: 87, Issue:1-2

    Neuropeptide Y (NPY) and peptide YY (PYY) are members of the pancreatic polypeptide family which have a high degree of primary and tertiary structural homology. They function as neurotransmitters and humoral agents in central nervous system and gastrointestinal function. During the last two decades, NPY body fluid concentrations and NPY/PYY brain receptor numbers have been demonstrated to be altered during the course of Alzheimer's disease. Recent research has shown that both NPY and PYY may be involved in aluminum metabolism in animal models. A brief discussion of the structure, biological activity and possible involvement of these peptides in aluminum metabolism and Alzheimer's disease is contained herein.

    Topics: Aluminum; Alzheimer Disease; Animals; Humans; Neuropeptide Y; Peptide YY; Protein Conformation

2001

Other Studies

1 other study(ies) available for peptide-yy and Alzheimer-Disease

ArticleYear
Satiety-related hormonal dysregulation in behavioral variant frontotemporal dementia.
    Neurology, 2014, Feb-11, Volume: 82, Issue:6

    To investigate whether patients with behavioral variant frontotemporal dementia (bvFTD) have dysregulation in satiety-related hormonal signaling using a laboratory-based case-control study.. Fifty-four participants (19 patients with bvFTD, 17 patients with Alzheimer disease dementia, and 18 healthy normal controls [NCs]) were recruited from a tertiary-care dementia clinic. During a standardized breakfast, blood was drawn before, during, and after the breakfast protocol to quantify levels of peripheral satiety-related hormones (ghrelin, cortisol, insulin, leptin, and peptide YY) and glucose. To further explore the role of patients' feeding abnormalities on hormone levels, patients were classified into overeating and nonovereating subgroups based on feeding behavior during separate laboratory-based standardized lunch feeding sessions.. Irrespective of their feeding behavior in the laboratory, patients with bvFTD, but not patients with Alzheimer disease dementia, have significantly lower levels of ghrelin and cortisol and higher levels of insulin compared with NCs. Furthermore, while laboratory feeding behavior did not predict alterations in levels of ghrelin, cortisol, and insulin, only patients with bvFTD who significantly overate in the laboratory demonstrated significantly higher levels of leptin compared with NCs, suggesting that leptin may be sensitive to particularly severe feeding abnormalities in bvFTD.. Despite a tendency to overeat, patients with bvFTD have a hormonal profile that should decrease food intake. Aberrant hormone levels may represent a compensatory response to the behavioral or neuroanatomical abnormalities of bvFTD.

    Topics: Aged; Alzheimer Disease; Biomarkers; Blood Glucose; Case-Control Studies; Feeding Behavior; Female; Frontotemporal Dementia; Ghrelin; Humans; Hydrocortisone; Hyperphagia; Insulin; Leptin; Male; Middle Aged; Neuropsychological Tests; Peptide YY

2014