International Journal of Pharmaceutical Investigation, 2019, 9, 4, 220-222.
DOI: 10.5530/ijpi.2019.4.41
Published: December 2019
Type: Short Communication
Authors:
Nishtha Singh
Department of Applied Science, Indian Institute of Information Technology, Allahabad, Deoghat, Jhalwa, Uttar Pradesh, INDIA.
Sonal Upadhyay
Department of Applied Science, Indian Institute of Information Technology, Allahabad, Deoghat, Jhalwa, Uttar Pradesh, INDIA.
Ankur Jaiswar
Department of Applied Science, Indian Institute of Information Technology, Allahabad, Deoghat, Jhalwa, Uttar Pradesh, INDIA.
Nidhi Mishra
Department of Applied Science, Indian Institute of Information Technology, Allahabad, Deoghat, Jhalwa, Uttar Pradesh, INDIA.
ABSTRACT
Background: Alzheimer’s Disease (AD) is a neuron related brain disorder leading to reasoning and memory loss. There is no specific cure identified for AD. JNK3 (c-Jun N-terminal kinase /stress-activated protein kinase) are highly revealed within the central nervous system, particularly neurons, playing vital role in functioning of brain. JNK3 hyper phosphorylation is a very common conclusion in neurodegenerative diseases. JNK3 in turn hyper phosphorylates Amyloid Precursor Protein (APP) which leads to the formation of Amyloid β peptides (an inductive agent of Alzheimer’s disease). Methods: Protein JNK-3 (PDB ID: 3KVX) was retrieved from protein data bank and later we docked a library of compounds against it. These were further validated by ADMET studies. Results: Thus, docking inhibitors of JNK3 may provide a promising sanitive approach. Based on best docking score and glide score a potential lead is identified against JNK3. Conclusion: Inhibiting JNK-3 may lead to less production of amyloidβ peptides, thus reducing the risk of Alzheimer’s disease.
Keywords: JNK3, Alzheimer’s disease, Amyloid β peptides.