Insulin signaling, glucose metabolism and mitochondria: Major players in Alzheimer's disease and diabetes interrelation

Many epidemiological studies have shown that diabetes, particularly type 2 diabetes, significantly increases the risk to develop Alzheimer's disease. Both diseases share several common abnormalities including impaired glucose metabolism, increased oxidative stress, insulin resistance and deposi...

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Bibliographic Details
Published in:Brain research 2012-03, Vol.1441, p.64-78
Main Authors: Correia, Sónia C, Santos, Renato X, Carvalho, Cristina, Cardoso, Susana, Candeias, Emanuel, Santos, Maria S, Oliveira, Catarina R, Moreira, Paula I
Format: Article
Language:English
Subjects:
Alzheimer disease
Alzheimer Disease - epidemiology
Alzheimer Disease - etiology
Alzheimer Disease - metabolism
Alzheimer's disease
Animals
brain
Cerebral glucose metabolism
Diabetes
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - epidemiology
Diabetes Mellitus, Type 2 - metabolism
epidemiological studies
glucose
Glucose - metabolism
Glucose - physiology
Humans
insulin
Insulin - adverse effects
Insulin - metabolism
Insulin - physiology
insulin resistance
Insulin signaling
metabolism
Mitochondria
Mitochondria - physiology
Neurology
noninsulin-dependent diabetes mellitus
Oxidative stress
proteins
risk
Risk Factors
Signal Transduction - physiology
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Summary:Many epidemiological studies have shown that diabetes, particularly type 2 diabetes, significantly increases the risk to develop Alzheimer's disease. Both diseases share several common abnormalities including impaired glucose metabolism, increased oxidative stress, insulin resistance and deposition of amyloidogenic proteins. It has been suggested that these two diseases disrupt common cellular and molecular pathways and each disease potentiates the progression of the other. This review discusses clinical and biochemical features shared by Alzheimer's disease and diabetes, giving special attention to the involvement of insulin signaling, glucose metabolism and mitochondria. Understanding the key mechanisms underlying this deleterious interaction may provide opportunities for the design of effective therapeutic strategies.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2011.12.063