Alzheimer's Disease Is Type 3 Diabetes - Evidence Reviewed

[Gert van der Hoek]

J Diabetes Sci Technol. 2008 Nov; 2(6): 1101?1113.

Abstract

Alzheimer's disease (AD) has characteristic histopathological, molecular, and biochemical abnormalities, including cell loss; abundant neurofibrillary tangles; dystrophic neurites; amyloid precursor protein, amyloid-β (APP-Aβ) deposits; increased activation of prodeath genes and signaling pathways; impaired energy metabolism; mitochondrial dysfunction; chronic oxidative stress; and DNA damage.

Gaining a better understanding of AD pathogenesis will require a framework that mechanistically interlinks all these phenomena. Currently, there is a rapid growth in the literature pointing toward insulin deficiency and insulin resistance as mediators of AD-type neurodegeneration, but this surge of new information is riddled with conflicting and unresolved concepts regarding the potential contributions of type 2 diabetes mellitus (T2DM), metabolic syndrome, and obesity to AD pathogenesis.

Herein, we review the evidence that (1) T2DM causes brain insulin resistance, oxidative stress, and cognitive impairment, but its aggregate effects fall far short of mimicking AD; (2) extensive disturbances in brain insulin and insulin-like growth factor (IGF) signaling mechanisms represent early and progressive abnormalities and could account for the majority of molecular, biochemical, and histopathological lesions in AD; (3) experimental brain diabetes produced by intracerebral administration of streptozotocin shares many features with AD, including cognitive impairment and disturbances in acetylcholine homeostasis; and (4) experimental brain diabetes is treatable with insulin sensitizer agents, i.e., drugs currently used to treat T2DM.

We conclude that the term ?type 3 diabetes? accurately reflects the fact that AD represents a form of diabetes that selectively involves the brain and has molecular and biochemical features that overlap with both type 1 diabetes mellitus and T2DM.


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[Gert van der Hoek]

Amy Berger can explain complicated things, so lay people (and doctors..) can understand. Great read.

Type 3 Diabetes: Metabolic Causes of Alzheimer’s Disease

July 8, 2014 by Amy Berger

As the population of the industrialized world ages, illnesses associated with aging consume a larger portion of our healthcare budgets and impose increasing burdens on the quality of life of patients and their caregivers. Estimates suggest that in the U.S., Alzheimer’s disease (AD) affects 12 percent of people over age 65 and nearly 50 percent of those over 85, with predictions for this to include 16 million people by 2050.1 National healthcare costs associated with AD are expected to surpass one trillion dollars by mid-century.1

Considering the fact that AD has no known cure and current therapies are largely ineffective, identifying the triggering mechanisms and exacerbating factors behind AD is of paramount importance, as prevention and early detection would serve to decrease—or at the very least delay—the physical, emotional and financial hardships this illness creates. Prevention is also critical because AD symptoms often do not appear until loss of functional neurons is so widespread that irreversible damage has already occurred.

The plethora of evidence linking hyperinsulinemia, T2D, mitochondrial dysfunction, and glucose dysregulation?all resulting from the refined, chemically manipulated modern Western diet? to Alzheimer?s disease suggests that the time has come for a drastic reevaluation of across-the-board recommendations for entire population groups to consume low-fat and low-cholesterol diets, which are, by default, high in carbohydrates.

Combined with stressful and sedentary lifestyles, and particularly when complicated by cholesterol-lowering medication, this amounts to nothing less than a blueprint for creating Alzheimer?s disease and other forms of neurological degeneration.

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[Shannon Bennett]

That was a fascinating read. Thanks Gert.