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Alzheimer’s disease and Type 2 Diabetes mellitus are distinct diseases with potential overlapping metabolic dysfunction upstream of observed cognitive decline.

Authors
  • Chornenkyy, Yevgen1
  • Wang, Wang-Xia1, 2
  • Wei, Angela3
  • Nelson, Peter T.1, 2
  • 1 University of Kentucky College of Medicine, Lexington, KY
  • 2 Sanders-Brown Center on Aging, Department of Pathology University of Kentucky, Lexington, KY
  • 3 Department of Biology, University of Kentucky
Type
Published Article
Journal
Brain Pathology
Publisher
Wiley (Blackwell Publishing)
Publication Date
Oct 09, 2018
Volume
29
Issue
1
Pages
3–17
Identifiers
DOI: 10.1111/bpa.12655
PMID: 30106209
PMCID: PMC6427919
Source
PubMed Central
Keywords
License
Unknown

Abstract

Alzheimer’s disease (AD) and type-2 diabetes mellitus (T2DM) are highly prevalent aging-related diseases associated with significant morbidity and mortality. Some findings in human and animal models have linked T2DM to AD-type dementia. Despite epidemiological associations between the T2DM and cognitive impairment, the inter-relational mechanisms are unclear. The preponderance of evidence in longitudinal studies with autopsy confirmation have indicated that vascular mechanisms, rather than classic AD-type pathologies, underlie the cognitive decline often seen in self-reported T2DM. T2DM is a known risk factor for cardiovascular and cerebrovascular disease (CVD), including increased risk of infarcts and small vessel disease in the brain and other organs. Furthermore, neuropathological examinations of post-mortem brains demonstrated evidence of cerebrovascular disease and little to no correlation between T2DM and β-amyloid deposits or neurofibrillary tangles. Nevertheless, the mechanisms upstream of early AD-specific pathology remain obscure. In this regard, there may indeed be overlap between the pathologic mechanisms of T2DM/”metabolic syndrome”, and AD. More specifically, cerebral insulin processing, glucose metabolism, mitochondrial function, and/or lipid metabolism could be altered in patients in early AD and directly influence symptomatology and/or neuropathology.

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