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Different Groups of People Deal With Different Symptoms


Alzheimer's & Diabetes

Updated: Feb 3, 2019


1. How does diabetes accelerate Alzheimer disease pathology?

Conclusions & Relevance: Alzheimer disease (AD) and diabetes are both associated with enormous and increasing socioeconomic effects. Diabetes affects the processing of amyloid-β and tau, and may increase the rate of formation of senile plaques and neurofibrillary tangles. Hyperinsulinemia is associated with amyloid-β accumulation and regulates tau phosphorylation. Oxidative stress activates inflammatory pathways and, hence, might exacerbate AD neuropathology. Mitochondrial dysfunction is associated with both diabetes and AD, and leads to intracellular calcium dysregulation and abnormal processing of the amyloid precursor protein. Induction of diabetes exacerbates AD neuropathology in mouse models of this neurodegenerative disease

Citation: Nature Reviews Neurology volume6, pages551–559 (2010)


2. Defective Insulin Signaling, and Mitochondrial Dysfunction as Common Molecular Denominators Connecting Type 2 Diabetes to Alzheimer Disease

Conclusion & Relevance: The emergence of molecular links between inflammatory, deregulated insulin signaling and mitochondrial dysfunction in AD and diabetes raises the prospect for development of novel therapeutic strategies for AD based on antidiabetes and/or anti-inflammatory agents

Citation: Fernanda G. De Felice and Sergio T. Ferreira.Diabetes 2014 Jun; DB_131954.


3. A Molecular Link between Type 2 Diabetes and Alzheimer Disease

Conclusion & Relevance: In summary, we show for the first time that formation of local IAPP amyloid (islet amyloid polypeptide) can be accelerated by hematogenous seed of synthetic IAPP and proIAPP fibrils. We also show that heterologous seeding with Aβ fibrils is possible. From our studies of patient material, we have found that islet IAPP amyloid does not recruit Aβ, but that cerebral Aβ amyloid contains IAPP.

Citation: The American Journal of Pathology.Volume 185, Issue 3, March 2015, Pages 834-846


4. Insulin as a bridge between type 2 diabetes and Alzheimer disease – how antidiabetics could be a solution for dementia.

Conclusion & Relevance: Type 2 diabetes patients often develop some form of dementia (such as AD), whereas AD patients may also present hyperglycemia, hypercholesterolemia, and insulin signaling dysfunction (common features to T2D). Thus, it has been increasingly suggested that several anti-T2D drugs may have a therapeutic potential in dementia, with some of them already under clinical analysis for that purpose. In fact, some of the above-mentioned anti-diabetics were beneficial against some AD hallmarks, e.g., Aβ plaque formation and tau hyperphosphorylation. Some of them also promoted neurogenesis and cell proliferation, and reduced neuroinflammation and cell death.

Citation: Front. Endocrinol., 08 July 2014.


5. Impaired Cerebral Autoregulation-A Common Neurovascular Pathway in Diabetes may Play a Critical Role in Diabetes-Related Alzheimer’s Disease

Conclusion & Relevance: AD and T2D are age dependent diseases. There are several potential mechanisms that have been proposed to be involved in the pathogenesis of AD including classical Aβ protein deposition, tau associated neurofibrillary tangles as well as the acetylcholine deficiency. Previous generations of treatment focusing on these mechanisms have failed to prevent the progression of AD, giving rise to the need for alternative therapeutic approaches. Recent studies have suggested that insulin resistance and cerebral autoregulation could be responsible for common pathogenesis in comorbid AD and Diabetes. It is possible that impaired autoregulation is occurring very early before the onset of dementia. Whether this cerebral vascular dysfunction precedes neurodegeneration or whether it is simply an outcome of amyloid and tau deposition has yet to be validated. In order to identify this pathology and even to develop therapeutic interventions there is a great need for more inclusive studies.

Citation: Curr Res Diabetes Obes J. 2017 Jun; 2(3): 555587.

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