How Insulin resistance and Glycogen Synthase Kinase

T2DM Type 2 Diabetes mellitus is characterised by elevated blood sugar levels caused by a lack of insulin, insulin resistance, or both. It has been related to the advent of secondary issues, which can result in a variety of morbidities.

Diabetes has been associated to a number of neurological diseases, including Alzheimer’s (AD). The evidence for a link between diabetes and Alzheimer’s disease is rising. Insulin signalling disruption has been discovered in the brain, resulting in increased tau protein phosphorylation (hyperphosphorylation), a characteristic and diagnostic of AD pathology, and the formation of neurofibrillary tangles (NFT).

 Insulin also promotes the formation of dendritic spines and synapse, the activation of neural stem cells, neurite growth and repair, and neuroprotection. This could explain why diabetics have a higher risk of developing Alzheimer’s disease as their diabetes advances and they get older. Interestingly, several in vivo studies in diabetic individuals using oral anti-diabetic medicines and insulin treatment demonstrated improved cognitive function and decreased tau hyperphosphorylation.

Insulin resistance in the brain is becoming more well recognised as a factor in the development of Alzheimer’s disease. Several studies have shown a strong relationship between insulin signalling and A metabolism. Insulin resistance is a characteristic of T2DM development and progression, and the Insulin Resistant and Glycogen Synthase Kinase is one of the primary causes of insulin insufficiency and resistance.


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