Neuroinflammation in Huntington’s & related neurodegenerative disorders

Abstract

One of the common pathological features of most age-related neurodegenerative disorders is the accumulation of abnormal protein deposits as inclusion bodies. It could be neuronal intranuclear inclusions in case of Huntington’s disease (HD), extracellular amyloid plaques, and intracellular neurofibrillary tangles in case of Alzheimer’s disease (AD), Lewy bodies in case of Parkinson’s disease (PD), and cytoplasmic inclusions in case of amyotrophic lateral sclerosis (ALS). Multiple mechanisms have been proposed to understand how these abnormal disease proteins induces neuronal dysfunction and neurodegeneration. However, neuroinflammation and oxidative stress are considered one of the most common phenomena that can be seen across all neurodegenerative disorders. Microglial cells play a key role in neuroinflammation. Continued activation of microglia and constant secretion of inflammatory molecules sets in the vicious cycle of inflammatory reactions in many of these neurodegenerative disorders. In this review we have focussed on the role of neuroinflammation in the pathogenesis of HD and other related neurodegenerative disorders.