Research Journal of Pharmacology and Pharmacodynamics

Ravi G. Patel ¹, Chirag K. Patel ¹, B. Panigrahi ¹, C. N. Patel ¹

Affiliations
1 Department of Pharmaceutical Chemistry, Shri Sarvajanik Pharmacy College, Hemchandracharya North Gujarat University, Arvind Baug, Mehsana-384001, Gujarat, IN

Abstract

Tuberculosis is an infection caused by the rod-shaped, non-spore-forming, aerobic bacterium Mycobacterium tuberculosis.Mycobacteria typically measure 0.5 im by 3 im, are classified as acid-fast bacilli, and have a unique cell wall structure crucial to their survival. The well developed cell wall contains a considerable amount of a fatty acid, mycolic acid, covalently attached to the underlying peptidoglycan-bound polysaccharide arabino galactan, providing an extraordinary lipid barrier. Mycobacterium tuberculosis is spread by small airborne droplets, called droplet nuclei, generated by the coughing, sneezing, talking, or singing of a person with pulmonary or laryngeal tuberculosis. These minuscule droplets can remain airborne for minutes to hours after expectoration. During the course of a systematic search for new antibiotics, an actinomycin complex was isolated from Streptomyces regensis sp. This actinomycin complex differs from other actinomycins described in literature in its amino acid composition and is very highly active against Staphylococcus aureus and Mycobacterium tuberculosis. The strains of Staph. aureus highly resistant to penicillin, streptomycin, chloramphenicol, tetracyclin and erythromycin are equally susceptible to its action.

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Chirag K. Patel ¹, B. Panigrahi ¹, R. Badmanaban ¹, C. N. Patel ¹

Affiliations
1 Department of Pharmaceutical Chemistry, Shri Sarvajanik Pharmacy College, Hemchandracharya North Gujarat University, Arvind Baug, Mehsana-384001, Gujarat, IN

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. β-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 β-secretase and γ-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 β-secretase to produce less amyoidogenic plaques. A second method aims at inhibiting γ-secretase activity on APP through allosteric inhibition of ATP binding.

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