Neuroimmune crosstalk and evolving pharmacotherapies in neurodegenerative diseases

Falguni Baidya, Mariya Bohra, Aishika Datta, Deepaneeta Sarmah, Birva Shah, Priya Jagtap, Swapnil Raut, Ankan Sarkar, Upasna Singh, Kiran Kalia, Anupom Borah, Xin Wang, Kunjan R. Dave, Dileep R. Yavagal, Pallab Bhattacharya

Research output: Contribution to journalReview articlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)160-178
Number of pages19
JournalImmunology
Volume162
Issue number2
DOIs
StatePublished - Feb 2021

Keywords

  • complement system
  • immune system
  • inflammasome
  • microglia
  • neurodegenerative disease

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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