Abstract
Both Alzheimer's disease (AD) and type 2 diabetes mellitus (DM) are two common forms of disease worldwide and many studies indicate that people with diabetes, especially DM, are at higher risk of developing AD. AD is characterized by progressive cognitive decline and accumulation of β-amyloid (Aβ) forming senile plaques. DM is a metabolic disorder characterized by hyperglycemia in the context of insulin resistance and relative lack of insulin. Both diseases also share common characteristics such as loss of cognitive function and inflammation. Inflammation resulting from Aβ further induces production of Aβ1-42 peptides. Inflammation due to overnutrition induces insulin resistance and consequently DM. Memory deficit and a decrease in GLUT4 and hippocampal insulin signaling have been observed in animal models of insulin resistance. The objective of this review was to show the shared characteristics of AD and DM.
Highlights
INTRODUCTIONMany researchers have struggled to understand the molecular basis of the pathophysiology of Alzheimer’s disease (AD) because an exponential number of cases have been predicted for the coming decades and more effective treatments will be required to prevent or halt progression of the disease
Many researchers have struggled to understand the molecular basis of the pathophysiology of Alzheimer’s disease (AD) because an exponential number of cases have been predicted for the coming decades and more effective treatments will be required to prevent or halt progression of the disease.AD is characterized by loss of cognitive function evolving to dementia and death
It should be highlighted that the disease onset occurs due to the accumulation of this protein, which leads to neuronal dysfunction and death.[21,22,23] β-amyloids are peptides of 39-43 amino acid residues[24] and, produced by most cells, there are no reports about their function.[25]
Summary
Many researchers have struggled to understand the molecular basis of the pathophysiology of Alzheimer’s disease (AD) because an exponential number of cases have been predicted for the coming decades and more effective treatments will be required to prevent or halt progression of the disease. Neocortex and hippocampus seem to be the areas most affected by specificity of the disease[12] and the loss of neurons in these areas is responsible for their atrophy, which is inherent to cognitive dysfunction, especially of memory, and the disease diagnosis.[16,17,18] Apart from these areas, the subcortical nuclei that connect the cortex are affected, including the cholinergic nucleus basalis of Meynert and medial septum.[12,19] β-amyloid protein is found diffusely in the brain of Alzheimer patients.[20] It should be highlighted that the disease onset occurs due to the accumulation of this protein, which leads to neuronal dysfunction and death.[21,22,23] β-amyloids are peptides of 39-43 amino acid residues[24] and, produced by most cells, there are no reports about their function.[25] It is derived from the amyloid precursor protein (APP),[26] which is cleaved in two pathways One of these occurs by the action of α- and γ-secretase enzymes and is non-amyloidogenic. It is known that the accumulation of Aβ together with
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