About this Research Topic
Endosomes have key roles in the sorting, trafficking, and recycling of proteins and lipids within cells. As endosomes transition from early endosomes to late endosomes, they fuse with lysosomes to complete degradation and recycling processes, thereby maintaining cellular homeostasis. Disruptions in the endo-lysosomal system are implicated in a range of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and lysosomal storage disorders. Recent scientific advancements have significantly improved our understanding of the role of endosomes and lysosomes in neuropathology. For example, mutations in LRRK2 impair lysosomal function in Parkinson’s disease, leading to the accumulation of toxic α-synuclein aggregates. In Alzheimer’s disease, presenilin 1 mutations disrupt lysosomal acidification, contributing to amyloid-β buildup. Additionally, activating Transcription factor EB (TFEB), a master regulator of lysosomal function, has been shown to enhance the clearance of toxic aggregates in neurodegenerative diseases. Advances in treatment strategies for lysosomal storage disorders, such as Niemann-Pick disease, further highlight the therapeutic potential of targeting lysosomal pathways.
Exosomes are small extracellular vesicles that originate from late endosomes, specifically multivesicular bodies (MVBs). Intraluminal vesicles (ILVs) within MVBs are either directed toward lysosomal degradation or secreted as exosomes when MVBs fuse with the plasma membrane. This process is tightly regulated and has critical implications in cellular communication, as well as the pathogenesis and progression of neurodegenerative diseases.
This Research Topic seeks to explore the molecular mechanisms underlying endosome and lysosome dysfunction in the brain, the impact of these alterations on neurodegenerative diseases, and the potential for therapeutic interventions targeting the endo-lysosomal system. We aim to enhance our understanding of the critical roles that endosomes and lysosomes play in neuropathology and highlight emerging approaches that may serve therapeutic interventions.
We invite contributions in the form of Original Research, Review, Mini Review, and Perspectives, focusing on but not limited to the following subtopics:
• The role of endosome and lysosome dysfunction in neurodegenerative disease progression
• The influence of exosomes on neurodegenerative disease progression
• Therapeutic strategies targeting endo-lysosomal pathways to mitigate neurodegeneration
Exosomes are small extracellular vesicles that originate from late endosomes, specifically multivesicular bodies (MVBs). Intraluminal vesicles (ILVs) within MVBs are either directed toward lysosomal degradation or secreted as exosomes when MVBs fuse with the plasma membrane. This process is tightly regulated and has critical implications in cellular communication, as well as the pathogenesis and progression of neurodegenerative diseases.
This Research Topic seeks to explore the molecular mechanisms underlying endosome and lysosome dysfunction in the brain, the impact of these alterations on neurodegenerative diseases, and the potential for therapeutic interventions targeting the endo-lysosomal system. We aim to enhance our understanding of the critical roles that endosomes and lysosomes play in neuropathology and highlight emerging approaches that may serve therapeutic interventions.
We invite contributions in the form of Original Research, Review, Mini Review, and Perspectives, focusing on but not limited to the following subtopics:
• The role of endosome and lysosome dysfunction in neurodegenerative disease progression
• The influence of exosomes on neurodegenerative disease progression
• Therapeutic strategies targeting endo-lysosomal pathways to mitigate neurodegeneration
Keywords: x
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.
