Abstract
Chronic diseases, as their name suggests, are progressive and can have overlapping features. Similar to this, Alzheimer's disease (AD) and diabetes mellitus (DM) fall into the category of chronic degenerative diseases. The global burden of these two ailments is manifold; hence, it seems important to view the pathophysiologic mechanisms of DM in the worsening of AD. Genetic as well as environmental factors are seen to play a role in the disease pathogenesis. Several genes, metabolic pathways, electrolytes, and dietary habits are seen to hasten brain atrophy. Lying behind this is the accumulation of amyloid precursor and tau - the misfolded proteins - within the brain substance. This mechanism is usually innate to AD itself, but the impact of insulin resistance, disturbing the homeostatic milieu, is seen as a powerful contributing factor aggravating the neuronal loss impairing an individual's memory. Since this neuronal loss is permanent, it may lead to complications as seen with AD. To reach a consensus, we conducted an electronic literature review search using different databases. This aided us in understanding the common aspects between AD and DM on genetic, molecular, cellular levels, as well as the impact of minerals and diet on the disease manifestation. We also found that despite exceptional work, additional efforts are needed to explore the relationship between the two entities. This will help physicians, researchers, and pharmaceuticals to frame remedies targeting the cause and avoid the progression of AD.
Highlights
BackgroundAlzheimer's disease (AD) is a chronic neurodegenerative disease leading to a progressive loss of neuronal tissue
Many researchers around the globe can signify many genes associated with single-nucleotide polymorphisms (SNP), various metabolic pathways, and alterations in the homeostatic milieu as a reason for the exacerbation in the brain atrophy in AD with type 2 diabetes mellitus (T2DM), especially with insulin resistance [2]
A study conducted by Silver et al identified genes such as AKT2, PIK3CB, IGF1R, PIK3CD, MTOR, IDE, AKT1S1, AKT1, which had a significant relation with the resistance of insulin on the brain, leading to cognitive impairment
Summary
Alzheimer's disease (AD) is a chronic neurodegenerative disease leading to a progressive loss of neuronal tissue. This leads to the accumulation of oligomers of A-beta in the memory zones of the brain, especially the hippocampus and the cortex [4]. Insulin resistance especially with T2DM may be a hidden risk factor for the progression of AD, increasing the susceptibility of the brain to A-beta proteins [14]. Methylation can lead to variable gene expressions in the POU3F2, KIF4B, and TMSL3 within the dopaminergic synapses and adenosine monophosphate-activated protein kinase (AMPK) pathways leading to the genetic connection of both the diseases [5]. A study conducted by Silver et al identified genes such as AKT2, PIK3CB, IGF1R, PIK3CD, MTOR, IDE, AKT1S1, AKT1, which had a significant relation with the resistance of insulin on the brain, leading to cognitive impairment. Some researchers used mouse genotype models to illustrate the tau phosphorylation in a diabetic environment, and this was pertinent with the imbalance of calcium, leading to impairment in the signaling within the cellular machinery [21]
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