Author(s):
Chirag K Patel, B Panigrahi, R Badmanaban, CN Patel.
Email(s):
Chirag.567@gmail.com
DOI:
Not Available
Address:
Chirag K. Patel*, B. Panigrahi , R. Badmanaban and C. N. Patel
Department of Pharmaceutical Chemistry, Shri Sarvajanik Pharmacy College, Hemchandracharya North Gujarat University, Arvind Baug, Mehsana-384001, Gujarat, India, Phone: 02762-247711
*Corresponding Author
Published In:
Volume - 2,
Issue - 1,
Year - 2010
ABSTRACT:
Alzheimer’s disease (AD) is a neurodegenerative disease caused by irregular protein formations in the brain leading to neuronal loss and ultimately affecting the patient’s cognitive ability and memory. AD affects nearly 4.5 million Americans, and this number is expected to continue to rise. The pathological manifestations of AD occur in the neurons and are two-fold; the primary cause is the accumulation.????amyloid (??amyloid precursor protein) depositions, which aggregate into pathogenic plaques. The second is the accumulation of paired helical filaments that form into neurofibrillary tangles (NFTs). Amyloid precursor protein plaques result from the sequential cleavage of the amyloid precursor protein (APP) by ??secretase and ??secretase. NFTs result from the hyperphosphorylation of tau, a stabilizing component of microtubules. Based on current understanding of the? Amyloid precursor protein pathway, two major strategies will be discussed that aim at decreasing the deposition of Amyloid precursor protein plaques in the brain. In the first approach, non-streroidal anti-inflammatory drugs alter the APP cleavage site by ??secretase to produce less amyoidogenic plaques. A second method aims at inhibiting ??secretase activity on APP through allosteric inhibition of ATP binding.
Cite this article:
Chirag K Patel, B Panigrahi , R Badmanaban, CN Patel. Biochemical Origins of Alzheimer’s Disease with Treatment Techniques. Research J. Pharmacology and Pharmacodynamics. 2010; 2(1):33-38.