Please use this identifier to cite or link to this item: http://dspace.dtu.ac.in:8080/jspui/handle/repository/18489
Title: PROMISING EFFECT OF REPURPOSED ANTI- HYPERGLYCEMIC DRUGS IN THE TREATMENT OF ALZHEIMER’S DISEASE
Authors: ARORA, VANSHIKA
Keywords: ANTI- HYPERGLYCEMIC DRUGS
ALZHEIMER’S DISEASE
DIABETES MELLITUS (DM)
AD MODEL ORGANISM
Issue Date: May-2021
Publisher: DELHI TECHNOLOGICAL UNIVERSITY
Series/Report no.: TD - 5320;
Abstract: Diabetes mellitus (DM) and Alzheimer's illness (AD) are both profoundly common circumstances in the older populace and significant general wellbeing trouble. Alzheimer's disease (AD) has trademark neuropathological anomalies, including localized degenerations of neurons, amyloid beta aggregation in brain tissue and neurofibrillary tangles, activating the genes that are pro- apoptotic, and leads to oxidative stress. Here the brain capacities keep on disintegrating, there is a decreasing face-to-face intellectual capacity, memory, artlessness, and socializing conduct. A system that successively interlinks every one of these wonders under one occasion is inadequate. Aggregating proof has demonstrated the vital functioning of insulin deficit and insulin obstruction as arbiters of Alzheimer’s degeneration of neurons. Thus, the inspection of the proof coming from the improvement of diabetes specialist prompted AD model organism. This phase appears to advance with AD to such an extent that, in the terminal stages, it declines and gets worldwide. APP-Aβ deposition, oxidative stress, impeded glucose and tau hyperphosphorylation and energy digestion all have been connected to annoyance in insulin/IGF flagging. We close that AD could also be alluded to as ''type III diabetes''. Also, inferable from normal pathophysiology with diabetes normal remedial system could be compelling for AD patients. The review will share detailed insights into pathological features and mechanisms of action of anti-diabetic drugs for the treatment of AD.
URI: http://dspace.dtu.ac.in:8080/jspui/handle/repository/18489
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