About this Research Topic
Amyloid-beta (Aβ) plays a central role in the pathogenesis of Alzheimer's disease (AD). Imbalance between Aβ production and clearance leads to Aβ deposition in brain and subsequent neuronal injury. Recent genome-wide association studies identified novel risk loci which are associated with immune system. Dysfunction of microglia, monocytes and T cells contributes to the pathogenesis of AD. Moreover, a panel of autoantibodies have been identified to be altered in AD patients and may participate in the pathogenesis of AD. Furthermore, recent evidences indicated meningeal lymphatic vessels play an important role in the drainage of Aβ and wastes out of the brain.
These findings all point to a consensus that immune system is involved in the pathogenesis of AD. Current potent therapeutic strategies are largely immune-based, although the results are disappointing. Therefore, further identification of immunological mechanisms of AD is of significance for understanding the complex network of AD pathogenesis and development of novel therapeutics for AD.
The goal of this Research Topic is to further understand immunological mechanisms of AD and to develop novel therapies for AD. Specifically, we welcome the submissions of Systematic Reviews, Meta-analyses, and Original Research articles focusing on, but not limited to, the following aspects:
• The role of peripheral immune cells in maintaining the hemostasis of Aβ
•. The role of humoral immunity in maintaining the hemostasis of Aβ
•. The role of autoantibodies in the pathogenesis of AD
•. Screening immune-based biomarkers for AD
•. Development of novel immunotherapies of AD
Keywords: Immune; Biomarker; Immunotherapy; Alzheimer
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