WORLD JOURNAL OF ADVANCE
HEALTHCARE RESEARCH

*Tanima Debnath Sarkar, John Anbumani Ganesan and P. Senthil Elango

ABSTRACT

In Parkinson's disease (PD), the degeneration of the substantia nigra disrupts the nigrostriatal pathway, leading toa reduction in striatal dopamine levels and the emergence of PD symptoms. While dopamine itself faceschallenges in crossing the blood-brain barrier, its precursor, levodopa, is capable of doing so. Levodopa undergoesabsorption in the small bowel and is swiftly broken down by aromatic-L-amino-acid decarboxylase (AADC) andcatechol-O-methyltransferase (COMT). Given that gastric AADC and COMT contribute to the degradation oflevodopa, the drug is administered alongside inhibitors of AADC (such as carbidopa or benserazide).Additionally, inhibitors of COMT are anticipated to see clinical use. The specific location of the decarboxylationof exogenous levodopa to dopamine in the brain remains unknown, but a significant portion of striatal AADC issituated in the nerve terminals of nigrostriatal dopaminergic pathways. Dopamine, synthesized and stored a newterminals and subsequently released which stimulates postsynaptic dopamine receptors, mediating theantiparkinsonian effects of levodopa. Dopamine agonists, in contrast, act directly on postsynaptic dopaminereceptors, eliminating the need for metabolic conversion, storage, and release. Parkinson disease protein7(PARK7) or Protein deglycase (DJ-1) is a gene responsible for hereditary recessive Parkinson's disease (PD). Thepotential inhibition of monoamine oxidase B (MAO-B) getting from chalcone in human body by adenosine A2Areceptor (AA2AR) antagonists has sparked interest in developing drugs that target both receptors. This dual-targetapproach holds promise for not only improving symptomatic relief but also potentially slowing the progression ofParkinson's disease (PD) by safeguarding against additional neurodegeneration.

[Full Text Article] [Download Certificate]