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Neuroimmune crosstalk and evolving pharmacotherapies in neurodegenerative diseases
Author(s) -
Baidya Falguni,
Bohra Mariya,
Datta Aishika,
Sarmah Deepaneeta,
Shah Birva,
Jagtap Priya,
Raut Swapnil,
Sarkar Ankan,
Singh Upasna,
Kalia Kiran,
Borah Anupom,
Wang Xin,
Dave Kunjan R.,
Yavagal Dileep R.,
Bhattacharya Pallab
Publication year - 2021
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.13264
Subject(s) - neurodegeneration , immune system , microglia , inflammasome , neuroinflammation , biology , neuroscience , innate immune system , complement system , crosstalk , immunology , inflammation , disease , medicine , pathology , physics , optics
Summary Neurodegeneration is characterized by gradual onset and limited availability of specific biomarkers. Apart from various aetiologies such as infection, trauma, genetic mutation, the interaction between the immune system and CNS is widely associated with neuronal damage in neurodegenerative diseases. The immune system plays a distinct role in disease progression and cellular homeostasis. It induces cellular and humoral responses, and enables tissue repair, cellular healing and clearance of cellular detritus. Aberrant and chronic activation of the immune system can damage healthy neurons. The pro‐inflammatory mediators secreted by chief innate immune components, the complement system, microglia and inflammasome can augment cytotoxicity. Furthermore, these inflammatory mediators accelerate microglial activation resulting in progressive neuronal loss. Various animal studies have been carried out to unravel the complex pathology and ascertain biomarkers for these harmful diseases, but have had limited success. The present review will provide a thorough understanding of microglial activation, complement system and inflammasome generation, which lead the healthy brain towards neurodegeneration. In addition to this, possible targets of immune components to confer a strategic treatment regime for the alleviation of neuronal damage are also summarized.