Advanced Glycation End Product Formation in Human Cerebral Cortex Increases With Alzheimer-Type Neuropathologic Changes but Is Not Independently Associated With Dementia in a Population-Derived Aging Brain Cohort
| Autor: | Stephen B. Wharton, Paul G. Ince, Thais Minett, Paul R. Heath, Pamela J. Shaw, Joanna J. Bury, C Richardson, Julie E. Simpson, Fiona E. Matthews, Claire J. Garwood, Carol Brayne, Annabelle Chambers |
|---|---|
| Přispěvatelé: | Brayne, Carol [0000-0001-5307-663X], Apollo - University of Cambridge Repository |
| Rok vydání: | 2020 |
| Předmět: |
Glycation End Products
Advanced Male medicine.medical_specialty Aging Population Plaque Amyloid Neuropathology Pathology and Forensic Medicine Cohort Studies 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Alzheimer Disease Internal medicine mental disorders Medicine Dementia Aging brain Humans Senile plaques education Advanced glycation end products 030304 developmental biology Aged Aged 80 and over Cerebral Cortex 0303 health sciences education.field_of_study business.industry Diabetes Neurofibrillary tangle Neurofibrillary Tangles General Medicine medicine.disease Endocrinology Neurology Ageing Female Neurology (clinical) Cerebral amyloid angiopathy Tau business Alzheimer’s disease 030217 neurology & neurosurgery |
| Popis: | Diabetes mellitus is a risk factor for dementia, and nonenzymatic glycosylation of macromolecules results in formation of advanced glycation end-products (AGEs). We determined the variation in AGE formation in brains from the Cognitive Function and Ageing Study population-representative neuropathology cohort. AGEs were measured on temporal neocortex by enzyme-linked immunosorbent assay (ELISA) and cell-type specific expression on neurons, astrocytes and endothelium was detected by immunohistochemistry and assessed semiquantitatively. Fifteen percent of the cohort had self-reported diabetes, which was not significantly associated with dementia status at death or neuropathology measures. AGEs were expressed on neurons, astrocytes and endothelium and overall expression showed a positively skewed distribution in the population. AGE measures were not significantly associated with dementia. AGE measured by ELISA increased with Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) neurofibrillary tangle score (p = 0.03) and Thal Aβ phase (p = 0.04), while AGE expression on neurons (and astrocytes), detected immunohistochemically, increased with increasing Braak tangle stage (p |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|