Author(s): M. Vijey Aanandhi, Yeshwanth Prasanna Kumar. B, Ranadheer Chowdary. P, Praveen. D

Email(s): hodpchemistry@velsuniv.ac.in

DOI: 10.5958/0974-360X.2018.00397.9   

Address: M. Vijey Aanandhi1*, Yeshwanth Prasanna Kumar. B2, Ranadheer Chowdary. P3, Praveen. D3
1Department of Pharmaceutical Chemistry and Analysis, School of Pharmaceutical Sciences, Vels University, (VISTAS) Chennai, India.
2Department of Pharmacy Practice. School of Pharmaceutical Sciences, Vels University, (VISTAS) Chennai, India.
3Research Scholar, School of Pharmaceutical Sciences, Vels University, (VISTAS) Chennai, India.
*Corresponding Author

Published In:   Volume - 11,      Issue - 5,     Year - 2018


ABSTRACT:
Alzheimer’s disease (AD) is the most common form of dementia. It characterized by the presence of numerous senile plaques and neurofibrillary tangles in the cerebral cortex and hippocampus of affected individuals. Mutations in the genes encoding presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein have been identified as the main genetic causes of familial AD. To date, more than 200 mutations have been described worldwide in PSEN1, which is highly homologous with PSEN2, while mutations in PSEN2 have been rarely reported.We performed a review of studies describing the mutations identified in PSEN1 and PSEN2. This article brings about the information pertaining to the role of presenilin and its derivatives in Alzheimer’s disease.


Cite this article:
M. Vijey Aanandhi, Yeshwanth Prasanna Kumar. B, Ranadheer Chowdary. P, Praveen. D. A Review on the Role of Presenilin in Alzheimer’s Disease . Research J. Pharm. and Tech 2018; 11(5):2149-2151. doi: 10.5958/0974-360X.2018.00397.9

Cite(Electronic):
M. Vijey Aanandhi, Yeshwanth Prasanna Kumar. B, Ranadheer Chowdary. P, Praveen. D. A Review on the Role of Presenilin in Alzheimer’s Disease . Research J. Pharm. and Tech 2018; 11(5):2149-2151. doi: 10.5958/0974-360X.2018.00397.9   Available on: https://www.rjptonline.org/AbstractView.aspx?PID=2018-11-5-82


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RNI: CHHENG00387/33/1/2008-TC                     
DOI: 10.5958/0974-360X 

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