Aggregation of misfolded proteins within cells can result in organelle damage and neuronal dysfunction, which are common pathological hallmarks of neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). Autophagy is one of the major mechanisms for the elimination of misfolded proteins and damaged organelles, and has been reported to be involved in the etiopathology of neurodegenerative diseases. Dysregulated autophagy can disrupt cellular homeostasis and lead to various disorders. For example, dysregulated autophagy in microglia can affect innate immune functions such as phagocytosis and inflammation, which contribute to the pathophysiology of age-related neurodegenerative diseases. Clarifying the mechanism of microglial autophagy would be a significant advancement in the achievement of on-demand microglia regulation as a potential therapeutic option in treating neurodegenerative diseases. A recent study discovered that the regulation of microglial polarization is relevant to neurodegenerative diseases, which inhibits the initiation of M1 inflammatory response cascades and promotes M2 polarization to protect neurons from neurotoxic substances.
Unfortunately, the lack of understanding of autophagy in microglia has prevented innovation until the last decade. The research on the ability to efficiently deliver drugs to the targeted regions in the brain is largely unknown; however, nanotechnology provides promising options for crossing the blood-brain barrier and achieving drug release in the brain. In-depth exploration of the specific mechanism of autophagy in microglia and relative regulation based on nanotechnology will have far-reaching significance for the targeted treatment of neurological diseases related to microglial activation.
This Research Topic aims to collect Original Research and high-quality Review articles that focus on molecular and cellular mechanisms of regulating microglial polarization and autophagy, as well as possible therapeutic strategies based on nanomedicines. Opinion articles will not be accepted.
Topics of interest include, but are not limited to:
? Role of microglia autophagy in Alzheimer's disease and other age-related neurodegenerative diseases
? Molecular and cellular mechanisms of autophagy-enhancing strategies to combat these disorders
? Modulation M1/M2 Polarization of microglia suppresses neuroinflammation
? Therapeutic strategies and clinical interventions, focusing on nanotechnology in the treatment of neurodegenerative disorders
Aggregation of misfolded proteins within cells can result in organelle damage and neuronal dysfunction, which are common pathological hallmarks of neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). Autophagy is one of the major mechanisms for the elimination of misfolded proteins and damaged organelles, and has been reported to be involved in the etiopathology of neurodegenerative diseases. Dysregulated autophagy can disrupt cellular homeostasis and lead to various disorders. For example, dysregulated autophagy in microglia can affect innate immune functions such as phagocytosis and inflammation, which contribute to the pathophysiology of age-related neurodegenerative diseases. Clarifying the mechanism of microglial autophagy would be a significant advancement in the achievement of on-demand microglia regulation as a potential therapeutic option in treating neurodegenerative diseases. A recent study discovered that the regulation of microglial polarization is relevant to neurodegenerative diseases, which inhibits the initiation of M1 inflammatory response cascades and promotes M2 polarization to protect neurons from neurotoxic substances.
Unfortunately, the lack of understanding of autophagy in microglia has prevented innovation until the last decade. The research on the ability to efficiently deliver drugs to the targeted regions in the brain is largely unknown; however, nanotechnology provides promising options for crossing the blood-brain barrier and achieving drug release in the brain. In-depth exploration of the specific mechanism of autophagy in microglia and relative regulation based on nanotechnology will have far-reaching significance for the targeted treatment of neurological diseases related to microglial activation.
This Research Topic aims to collect Original Research and high-quality Review articles that focus on molecular and cellular mechanisms of regulating microglial polarization and autophagy, as well as possible therapeutic strategies based on nanomedicines. Opinion articles will not be accepted.
Topics of interest include, but are not limited to:
? Role of microglia autophagy in Alzheimer's disease and other age-related neurodegenerative diseases
? Molecular and cellular mechanisms of autophagy-enhancing strategies to combat these disorders
? Modulation M1/M2 Polarization of microglia suppresses neuroinflammation
? Therapeutic strategies and clinical interventions, focusing on nanotechnology in the treatment of neurodegenerative disorders
