Drug Res (Stuttg) 2023; 73(05): 247-250
DOI: 10.1055/a-2015-8041
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Receptor for Advanced Glycation End Products: Dementia and Cognitive Impairment

Aditya Singh
1   Department of Pharmacy, Faculty of Pharmacy, Integral University, Lucknow, India
,
Vaseem Ahamad Ansari
1   Department of Pharmacy, Faculty of Pharmacy, Integral University, Lucknow, India
,
Tarique Mahmood
1   Department of Pharmacy, Faculty of Pharmacy, Integral University, Lucknow, India
,
Farogh Ahsan
1   Department of Pharmacy, Faculty of Pharmacy, Integral University, Lucknow, India
,
Rufaida Wasim
1   Department of Pharmacy, Faculty of Pharmacy, Integral University, Lucknow, India
,
Mohammad Shariq
1   Department of Pharmacy, Faculty of Pharmacy, Integral University, Lucknow, India
,
Saba Parveen
1   Department of Pharmacy, Faculty of Pharmacy, Integral University, Lucknow, India
,
Shubhrat Maheshwari
2   Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Rama University, Mandhana, Bithoor Road, Kanpur, Uttar Pradesh, India
› Author Affiliations
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Abstract

The pathophysiological processes of dementia and cognitive impairment are linked to advanced glycation end products (AGEs) and their receptor (RAGE).The neurofibrillary tangles (NFTs) of abnormally hyperphosphorylated tau protein and senile plaques (SPs), which are brought on by amyloid beta (Aβ) deposition, are the hallmarks of Alzheimer’s disease (AD), a progressive neurodegenerative condition. Advanced glycation end products that are produced as a result of vascular dysfunction are bound by the receptor for advanced glycation end products (RAGE). Dementia and cognitive impairment could develop when RAGE binds to Aβ and produces reactive oxygen species, aggravating Aβ buildup and ultimately resulting in SPs and NFTs. RAGE could be a more powerful biomarker than Aβ because it is implicated in early AD. The resident immune cells in the brain known as microglia are essential for healthy brain function. Microglia is prominent in the amyloid plaques’ outside border as well as their central region in Alzheimer’s disease. Microglial cells, in the opinion of some authors, actively contribute to the formation of amyloid plaques. In this review, we first discuss the early diagnosis of dementia and cognitive impairment, and then detail the interaction between RAGE and Aβ and Tau that is necessary to cause dementia and cognitive impairment pathology, and it is anticipated that the creation of RAGE probes will help in the diagnosis and treatment of dementia and cognitive impairment.



Publication History

Received: 05 January 2023

Accepted: 17 January 2023

Article published online:
08 March 2023

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