Version 1
: Received: 23 July 2019 / Approved: 24 July 2019 / Online: 24 July 2019 (08:05:52 CEST)
Version 2
: Received: 6 September 2019 / Approved: 9 September 2019 / Online: 9 September 2019 (06:12:15 CEST)
How to cite:
Hayden, M.R. Type 2 Diabetes Mellitus Increases The Risk of Late-Onset Alzheimer’s Disease: Obesity, Aging, Intersects and Continuum Of Progression. Preprints2019, 2019070265. https://doi.org/10.20944/preprints201907.0265.v1
Hayden, M.R. Type 2 Diabetes Mellitus Increases The Risk of Late-Onset Alzheimer’s Disease: Obesity, Aging, Intersects and Continuum Of Progression. Preprints 2019, 2019070265. https://doi.org/10.20944/preprints201907.0265.v1
Hayden, M.R. Type 2 Diabetes Mellitus Increases The Risk of Late-Onset Alzheimer’s Disease: Obesity, Aging, Intersects and Continuum Of Progression. Preprints2019, 2019070265. https://doi.org/10.20944/preprints201907.0265.v1
APA Style
Hayden, M.R. (2019). Type 2 Diabetes Mellitus Increases The Risk of Late-Onset Alzheimer’s Disease: Obesity, Aging, Intersects and Continuum Of Progression. Preprints. https://doi.org/10.20944/preprints201907.0265.v1
Chicago/Turabian Style
Hayden, M.R. 2019 "Type 2 Diabetes Mellitus Increases The Risk of Late-Onset Alzheimer’s Disease: Obesity, Aging, Intersects and Continuum Of Progression" Preprints. https://doi.org/10.20944/preprints201907.0265.v1
Abstract
Type 2 diabetes mellitus (T2DM) and late-onset Alzheimer’s disease-dementia (LOAD) have become parallel global pandemics and current predictions indicate they will only increase over the coming decades. These pandemics may result from the coexistent increase of obesity and aging. T2DM is associated with cognitive impairments associated with both metabolic factors, diabetic cognopathy (DC) and an increased risk of LOAD. This review addresses possible mechanisms due to obesity, aging, intersects and mechanisms for the continuum of progression. Multiple ultrastructural images in female diabetic db/db models are utilized to demonstrate marked cellular remodeling changes and provide for the discussion of functional changes in T2DM. Throughout this review multiple endeavors to demonstrate how T2DM increases the vulnerability of the brain’s neurovascular unit (NVU), neuroglia and neurons are presented. It is difficult to condense so many links between T2DM and LOAD; however, five major intersections could be considered: i. aging (chronic age-related diseases); ii. metabolic (hyperglycemia - advanced glycation end-products and its receptor (AGE/RAGE) interactions and hyperinsulinemia – insulin resistance (a linking linchpin); iii. oxidative stress (reactive oxygen-nitrogen species); iv. inflammation (peripheral macrophage and central brain microglia); v. vascular (macrovascular accelerated atherosclerosis - vascular stiffening and microvascular NVU remodeling with resulting impaired cerebral blood flow).
Medicine and Pharmacology, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
