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Abstract
Neuroinflammation is recognized as a key contributor to the pathogenesis of Alzheimer's disease and Parkinson's disease.
- Neuroinflammation occurs throughout various stages of Alzheimer's and Parkinson's diseases, increasing in complexity.
- Endogenous pathological triggers, such as amyloid-β peptide, hyperphosphorylated tau, and α-synuclein, activate glial cells, leading to chronic neuroinflammation that may worsen neurodegeneration.
- Peripheral factors, including systemic inflammation, environmental exposures, and gut-brain interactions, could influence neuroinflammatory responses.
- The roles of oligodendrocyte precursor cells and oligodendrocytes in neuroimmune interactions are increasingly recognized.
- Advanced methodologies like glial cell imaging and single-cell transcriptomics are enhancing understanding of the mechanisms behind neuroinflammation.
- Emerging therapeutic strategies targeting neuroinflammatory pathways may offer potential for developing disease-modifying treatments for Alzheimer's and Parkinson's diseases.
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