Signal Transduction Abnormalities in Alzheimer’s Disease
The article defines Alzheimer’s Disease as a neurodegenerative disorder with progressive dementia that results due to two significant changes in brain structure, which are intracellular protein deposits NFT (neurofibrillary tangles) and extracellular proteins deposits bounded by dystrophic neurites containing senile plagues. In the article, traits of phenotype changes of cells that are undergoing cell division are portrayed by hippocampal and select cortical neuronal in diseases of Alzheimer’s. The article describes if components that are responsible for triggering cellular proliferation and differentiation, as well as kinase pathway activation, contributes to signal transduction cascade activation in a disease of Alzheimer’s. Also, the article describes the implication of proteins in signal transduction from cell-surface receptors through the pathway of ras. Comparison is made between age-matched controls and the disease of Alzheimer during transduction. It is also depicted that in the article, the author evaluates the degree of alteration of ras pathways and gives suggestions on what might be resulting as well as the role of neuronal signaling. Both causative and consequential events are explored, and disease mechanisms examined in detail. The study also describes signal transduction, its impact in the body, and the process of transmission as well as its defects.
(Keywords: Alzheimer’s disease; ras pathways; signal transduction; cell cycle; pathogenesis; and pathology)
Reference
Nguyen, T. V. V., Galvan, V., Huang, W., Banwait, S., Tang, H., Zhang, J., & Bredesen, D. E. (2008). Signal transduction in Alzheimer disease: p21‐activated kinase signaling requires C‐terminal cleavage of APP at Asp664. Journal of neurochemistry, 104(4), 1065-1080. Work retrieved on 20/02/2020 from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2553705/