Published Paper Details:

A build-up of senile plaques (SPs) and neurofibrillary tangles (NFTs) in the brain is the pathological hallmark of Alzheimer's disease (AD), the primary cerebrovascular illness that causes dementia. Diabetes mellitus is a condition marked by improper carbohydrate metabolism and increased blood glucose levels. It is caused by a malfunction in the body's capacity to create or respond to the hormone insulin. There is growing recognition that cognitive impairment is a significant comorbidity of diabetes mellitus. There are many stages of diabetes-related cognitive impairment, each with unique cognitive characteristics, affected age groups and prognoses, and most likely distinct underlying processes. Additionally, mounting data points to a number of linkages between the neuropathology underlying DM and AD, and evidence even points to the possibility that experimental production of DM might result in cognitive failure, even in rodent animal models. Deficits in spatial learning are correlated with unique modifications in hippocampus synaptic plasticity in animal models of diabetes. Although the complex pathophysiology of diabetic encephalopathy is not fully known, it is evident that it has characteristics with the pathophysiology of diabetic neuropathy and brain aging. Chronic hyperglycemia-related alterations in metabolism and blood vessels are present, and there may also be abnormalities in the brain's ability to use insulin. Thus, insulin treatment may have a direct impact on the brain in addition to addressing hyperglycemia. Therefore, insulin therapy may have a direct impact on the brain in addition to treating hyperglycemia. It is not yet known why AD typically occurs in older people, despite genetic research demonstrating that the primary component of SPs, ?-amyloid peptide (A?), is the critical element causing AD pathogenesis.