Biology of Parkinsonism to enhance lifespan of mitochondria in Parkinson's patients

Al-Baraa Akram El-Sayed

Faculty of health and life sciences, department of pharmaceutical biotechnology, Portland laboratory in De Montfort University in Leicester (United Kingdom)

Abstract

Lewy bodies and a noticeable loss of dopaminergic neurons in the substantia nigra are the two main symptoms of Parkinson's disease, which is a diverse, multifaceted, and frequently complex illness. Parkinson's disease also causes motor disability.

Although the precise PD pathophysiology is still being researched, one of the key pathogenic pathways thought to underlie PD development is mitochondrial dysfunction. Based on the premise that representations of HtrA2 (the mitochondrial precursor serine protease gene) might help to increase mitochondrial stress and transcriptional activation of the CHOP gene in response to nuclear stress. The goal of this article  was to examine, through laboratory-based research, the function of HtrA2 and CHOP in stress signaling transmission and the ensuing activation of mitochondrial quality control in Parkinson's disease.

Keywords: Parkinson's disease, HtrA2, mitochondrial stress