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Neuroinflammation and Neuroimmunomodulation in Alzheimer’s Disease

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机构： [1]Department of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tian Tan Hospital, Capital Medical University, Beijing 100050, China [2]Department of Neurology, Northern Jiangsu People’s Hospital, Clinical Medical College of Yangzhou University, Yangzhou 225001, Jiangsu Province, China [3]Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, School of Medicine, Yangzhou University, Yangzhou 225001, Jiangsu, China

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关键词： Alzheimer’s disease Amyloid β Inflammasome Neuroinflammation

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Purpose of Review: This review provides an updated summary of our current understanding of the role of neuroinflammation in Alzheimer’s disease (AD). We introduce the main cellular and molecular players in AD-related neuroinflammation, highlight the latest discovery on how inflammasome participates in the development of AD, and discuss potential neuroimmunomodulation approaches for AD prevention and therapy. Recent Findings: AD is characterized by the abnormal accumulation or aggregation of proteins such as amyloid β (Aβ) and tau, which could act as danger-associated molecular patterns that engage pattern-recognition receptors to activate inflammatory signaling pathways and promote the production and release of a variety of inflammatory mediators. While the role of neuroinflammatory response in AD is complex and poorly understood, it is generally considered that consistent neuroinflammation has detrimental effects and facilitate the progression of AD. In particular, recent evidence suggests that targeting Nod-like receptor protein 3 (NLRP3) inflammasome could slow the deposition of Aβ plaques in the brain and improve neurological outcome in AD patients. Summary: Neuroinflammation plays an important role in AD. Further elucidation of molecular mechanisms underlying AD-related neuroinflammatory response would help develop novel strategies for the prevention and treatment of AD. © 2018, Springer Nature Switzerland AG.

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第一作者机构： [1]Department of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tian Tan Hospital, Capital Medical University, Beijing 100050, China

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通讯机构： [1]Department of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tian Tan Hospital, Capital Medical University, Beijing 100050, China [2]Department of Neurology, Northern Jiangsu People’s Hospital, Clinical Medical College of Yangzhou University, Yangzhou 225001, Jiangsu Province, China [3]Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, School of Medicine, Yangzhou University, Yangzhou 225001, Jiangsu, China

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