作者: Cinzia Volonte , Chiara Parisi , Savina Apolloni
DOI: 10.2174/1871527314666150225143921
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摘要: Results from amyotrophic lateral sclerosis (ALS) patients and pre-clinical studies strongly suggest that systemic CNS-intrinsic immune activation plays a central role in ALS pathogenesis. Microglial cells are emerging this context as master regulators with bi-functional the progression of the pathological response. They foster pro-inflammatory setting through the production cytotoxic cytokines chemokines (M1 phenotype), after an aborted effort to sustain an anti-inflammatory environment for motor neurons release beneficial and growth factors (M2 phenotype). In review, we gather information meant propose histamine and ATP, which released mast cells, microglia damaged at sites injury where they function as transmitters, have be considered new players neuroinflammatory arena. After all, abnormal histamine and ATP signalling brain already documented neurodegenerative/neuroinflammatory conditions such multiple sclerosis, Alzheimer Parkinson's disease and, present, histamine- well ATP-related compounds clinical trial these same pathologies. Concerning ALS, while data now available about purinergic mechanisms, the involvement is basically unexplored. The circumstantial evidence present here thus constitutes a solid background formulating novel hypotheses, stimulating scientific debate most inspiring future research. We deem potential neuroinflammation might find fertile ground thrive. still without cure: why not play kid on block?