Molecular and Cellular Insights: Neuroinflammation and Amyotrophic Lateral Sclerosis

摘要: Accumulation of misfolded and abnormal proteins generates probably a common complex pathomechanism in various neurodegenerative diseases (Alzheimer’s, Parkinson’s, Huntington’s, Amyotrophic Lateral Sclerosis, Prion) aging. In amyotrophic lateral sclerosis (ALS), neuroinflammation appears the form T-lymphocyte infiltration, presence reactive astroglial microglial cells. Most likely, end stage this toxic cascade results death motor neurons cortex, brainstem, spinal cord. More than 10 different genetic causes familial ALS are known; but still it is challenge to prevent loss descending tracts by suppressing degeneration neurons. This chapter will focus on precise understanding neuroinflammatory responses molecular also discusses new potential therapeutic strategies improve neuroprotection alleviate proteotoxicity linked neurodegeneration.