Author/Authors :
Kumar Jha، Saurabh نويسنده Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly DCE), Delhi, India. Kumar Jha, Saurabh , Kumar Jha، Niraj نويسنده Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly DCE), Delhi, India. Kumar Jha, Niraj , Kar، Rohan نويسنده Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly DCE), Delhi, India. Kar, Rohan , Ambasta، Rashmi K نويسنده Molecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly DCE), Delhi, India. Ambasta, Rashmi K , Kumar، Pravir نويسنده ,
Abstract :
Parkinsonʹs disease (PD) is a chronic neurodegenerative condition which has the second largest incidence rate
among all other neurodegenerative disorders barring Alzheimerʹs disease (AD). Currently there is no cure and
researchers continue to probe the therapeutic prospect in cell cultures and animal models of PD. Out of the
several factors contributing to PD prognosis, the role of p38 MAPK (Mitogen activated protein-kinase) and
PI3K/AKT signalling module in PD brains is crucial because the impaired balance between the pro- apoptotic
and anti-apoptotic pathways trigger unwanted phenotypes such as microglia activation, neuroinflammation,
oxidative stress and apoptosis. These factors continue challenging the brain homeostasis in initial stages thereby
essentially assisting the dopaminergic (DA) neurons towards progressive degeneration in PD. Neurotherapeutics
against PD shall then be targeted against the misregulated accomplices of the p38 and PI3K/AKT cascades. In
this review, we have outlined many such established mechanisms involving the p38 MAPK and PI3K/AKT
pathways which can offer therapeutic windows for the rectification of aberrant DA neuronal dynamics in PD
brains.
