Authors : Madhu S.U, Hariprasad M.G, N C. Nagalakshmi, Harshitha Arun Pardhe
DOI : 10.18231/j.ijn.2020.002
Volume : 6
Issue : 1
Year : 2020
Page No : 6-13
Neurodegeneration is a condition which defined by a inflammation or damage of neuron and demyelination.
It is characterized through the permeability of the Blood Brain Barrier (BBB), the myelin sheath damage,
axon damage, the formation of glial scar and the presence of inflammatory cells. The brain is one of the
organs specifically liable to the effects of reactive oxygen species (ROS) due to its high oxygen demand and
its profusion of peroxidation-susceptible lipid cells. Neurodegeneration includes intracellular processes like
oxidative damage, proteasome,dysfunction of mitochondrial, apoptosis (cell death), autophagy, Inactivating
of the c-Jun N-terminal kinase (JNK) pathway leads to axon degeneration and the common pathology
of neurodegeneration consists of deposition of proteins missfolding such as , a-synuclein in Parkinson’s
disease (PD), transactive response DNA binding protein 43 (TDP-43) in dementia, amyloid-b (Ab ) in
Alzheimer’s disease. The incidence of neurodegenerative diseases which are wide-ranging of Alzheimer’s
disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease
(HD), Fronto temporal dementia (FTD). Oxidative stress is caused by an imbalanced redox states, relating
either excessive generation of ROS or dysfunction of the antioxidant system.
Keywords: Neurodegenerative diseases, Reactive oxygen species (ROS), Neurodegeneration excitotoxicity, Protein miss folding, Neurotoxicity