World Journal of
Pharmaceutical and Life Sciences

An International Peer Reviewed Journal for Pharmaceutical and Life Sciences
An Official Publication of Society for Advance Healthcare Research (Reg. No. : 01/01/01/31674/16)
World Journal of Pharmaceutical and Life Sciences (WJPLS) has indexed with various reputed international bodies like : Google Scholar, Index Copernicus, Indian Science Publications, SOCOLAR, China, Cosmos Impact Factor, Research Bible, Fuchu, Tokyo. JAPAN, Scientific Indexing Services (SIS), Jour Informatics (Under Process), UDLedge Science Citation Index, Global Impact Factor (In Process), International Impact Factor Services, International Scientific Indexing, UAE, International Society for Research Activity (ISRA) Journal Impact Factor (JIF), Science Library Index, Dubai, United Arab Emirates, International Innovative Journal Impact Factor (IIJIF), Scientific Journal Impact Factor (SJIF), Eurasian Scientific Journal Index (ESJI), Indian citation Index (ICI), 

Abstract

BIOCHEMISTRY OF ALZHEIMER’S DISEASE

Dr. Anil Batta*

ABSTRACT

Alzheimer's disease, the cause of one of the most common types of dementia, is a brain disorder affecting the elderly and is characterized by the formation of two main protein aggregates: senile plaques and neurofibrillary tangles, which are involved in the process leading to progressive neuronal degeneration and death. Neurodegeneration in Alzheimer's disease is a pathologic condition of cells rather than an accelerated way of aging. The senile plaques are generated by a deposition in the human brain of fibrils of the beta-amyloid peptide (Abeta), a fragment derived from the proteolytic processing of the amyloid precursor protein (APP). Tau protein is the major component of paired helical filaments (PHFs), which form a compact filamentous network described as neurofibrillary tangles (NFTs).[1] Experiments with hippocampal cells in culture have indicated a relationship between fibrillary amyloid and the cascade of molecular signals that trigger tau hyperphosphorylations. Furthermore, the degree of dementia is clearly associated more with the degree of neurofibrillary pathology than with the amyloid plaque burden. In general, amyloid formation may very well be at the end of a pathophysiological cascade, set in motion by many different triggers. This cascade could involve excessive apoptosis, followed by necrosis and inflammation.[2] The pathogenesis of AD is complicated, but further identification of the processes of neurodegeneration will also lead to identification of the factors that make specific neurons vulnerable and, hopefully, point the way to a means to prevent neuronal degeneration at an early stage.

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