About this Research Topic
Neurodegenerative diseases are characterized by the progressive death of neurons that cause neurological and neuropsychological symptoms, including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), etc. Multi-factors of external environmental and internal genetic risk factors are related to the diseases. However, a clear mechanism is still elusive, and effective therapeutics are not at hand. Protein misfolding and propagation are the major hallmarks of several neurodegenerative diseases, which can activate pattern recognition receptors that are expressed by innate immune cells of the brain, generating pro-inflammatory cytokines, chemokines, complement components, and free radicals.
This Research Topic aims to explore the mechanisms of protein misfolding and propagation, and identify their connection to innate immunity in neurodegenerative diseases. We believe that elucidating how protein misfolding activates microglial and astroglia cells, promotes the formation of NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasomes, causes neuronal dysfunction, generates pro-inflammatory cytokines and autoantibodies, and leads to downstream biophysical effects will facilitate the etiology elucidation and therapeutic development for neurodegenerative diseases, as well as provide new insight into biomarker discovery. We also aim to study the mechanism of protein propagation and neuroinflammation, especially at the early stage of neurodegenerative disease.
This Research Topic will focus on understanding the molecular mechanisms of protein misfolding, propagation, and innate immunity in neurodegenerative disorders. We are interested in proteins including amyloid-beta, tau, alpha-synuclein, prion, TDP-43 proteins, etc. We cordially invite authors and investigators within this complex field of universal interest, to submit original research or review articles regarding, but not limited to the following areas:
• Mechanisms of microglial and astroglia cells 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 autoantibodies 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
This Research Topic aims to explore the mechanisms of protein misfolding and propagation, and identify their connection to innate immunity in neurodegenerative diseases. We believe that elucidating how protein misfolding activates microglial and astroglia cells, promotes the formation of NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasomes, causes neuronal dysfunction, generates pro-inflammatory cytokines and autoantibodies, and leads to downstream biophysical effects will facilitate the etiology elucidation and therapeutic development for neurodegenerative diseases, as well as provide new insight into biomarker discovery. We also aim to study the mechanism of protein propagation and neuroinflammation, especially at the early stage of neurodegenerative disease.
This Research Topic will focus on understanding the molecular mechanisms of protein misfolding, propagation, and innate immunity in neurodegenerative disorders. We are interested in proteins including amyloid-beta, tau, alpha-synuclein, prion, TDP-43 proteins, etc. We cordially invite authors and investigators within this complex field of universal interest, to submit original research or review articles regarding, but not limited to the following areas:
• Mechanisms of microglial and astroglia cells 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 autoantibodies 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
Keywords: neurodegenerative diseases, neuroinflammation, amyloid-beta, tau, alpha-synuclein, prion, TDP-43, anti-inflammation drugs, inflammasome, microglia activation
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
