Document Type : Original Article
Authors
1
biochemistry department,faculty of Pharmacy,Suez Canal University, EGYPT
2
Biochemistry department,Faculty of Pharmacy - Suez Canal University, Egypt
3
biochemistry department, faculty of pharmacy, suez canal university, Egypt
4
Biochemistry department, Faculty of Pharmacy, Suez Canal University, Ismailia, 41522, Egypt
5
Biochemistry department, Faculty of Pharmacy, Ahram Canadian University, October 6 City, EGYPT
Abstract
Type 2 diabetes mellitus (T2DM) is a common disease in the elderly, affecting around 20% of geriatrics. In cross-sectional studies, T2DM had various adverse health effects, including cognitive impairment. The association of T2DM with decreased cognitive function suggests that T2DM can contribute to Alzheimer's disease (AD)
The relationship between T2DM and AD continues to grow rapidly. It has been suggested that AD can be considered "type 3 diabetes”. Along with the processing of amyloid precursor protein (APP) and tau phosphorylation, the molecular links between T2DM and AD provide clues for new therapeutic targets such as glucagon-like peptide-1 (GLP-1), butyrylcholinesterase and receptor for advanced glycosylation end products (AGE).
A possible mechanism correlating T2DM and AD is the alteration in insulin signaling in the brain. Insulin signaling is involved in several neuronal functions, and plays a vital role in the pathophysiology of AD. Therefore, the modification of neuronal insulin signaling by diabetic conditions may contribute to AD progression. Another possible mechanism is cerebrovascular changes, a common pathological change observed in both diseases. The importance of amyloid beta peptide (Aβ) induced cerebrovascular dysfunction in AD has been reported, indicating that pathological interactions between AGE receptor and Aβ have a role in this disorder.
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