Neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD), are marked by the progressive loss of neurons, leading to severe neurological and neuropsychological symptoms. Despite extensive research, the precise mechanisms underlying these diseases remain elusive, and effective treatments are still lacking. A significant area of interest is the role of protein misfolding and propagation, which are key features in several neurodegenerative disorders. These misfolded proteins can activate pattern recognition receptors in the brain's innate immune cells, leading to the production of pro-inflammatory cytokines, chemokines, complement components, and free radicals. Recent studies have begun to unravel the complex interactions between protein misfolding and neuroinflammation, yet many questions remain unanswered. Understanding these processes is crucial for developing new therapeutic strategies and identifying potential biomarkers for early diagnosis.

This research topic aims to delve into the mechanisms of protein misfolding and propagation and their connection to innate immunity in neurodegenerative diseases. We seek to elucidate how protein misfolding activates microglial and astroglial cells, promotes the formation of NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasomes, and contributes to neuronal dysfunction and the generation of pro-inflammatory cytokines and autoantibodies. By exploring these pathways, we hope to advance the understanding of the etiology of neurodegenerative diseases and facilitate the development of novel therapeutic approaches. Additionally, we aim to investigate the mechanisms of protein propagation and neuroinflammation, particularly during the early stages of these diseases.

To gather further insights into the molecular mechanisms of protein misfolding, propagation, and innate immunity in neurodegenerative disorders, we welcome articles addressing, but not limited to, the following themes:
- Mechanisms of microglial and astroglial cell activation caused by misfolded proteins
- The relationship between protein propagation and the development of NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome
- How misfolded proteins drive neuronal dysfunction and contribute to cell death
- Mechanisms of autoantibody generation caused by protein misfolding and propagation
- The mechanism of neuroinflammation at the early stage of neurodegenerative disease
- Diagnostic and therapeutic strategies targeting the mechanisms that drive protein misfolding

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Unraveling Protein Misfolding and Innate Immunity in Neurodegenerative Diseases

Topic Coordinator