近日，中南大学湘雅医院国家老年疾病临床医学研究中心唐宇副教授受《Current Alzheimer Research》（IF=3.047）编辑部邀请，担任该杂志的客座主编，组织一项关于阿尔兹海默症（Alzheimer's disease，AD）免疫发病机制的研究专题（详情见后）。《Current Alzheimer Research》是著名出版社Bentham Science旗下的重要刊物，主要发表有关AD与其他常见老年性痴呆、神经退行性疾病领域的前沿综述和原创性研究，助力于探讨AD的神经生物学、遗传学、发病机制、治疗策略以及药物临床试验研究等。该专刊目前正在进行稿件的征集工作，已经邀请到来自中国、美国等多个国家和地区的学者，并热烈欢迎更多的专家同仁积极投稿。
Special Thematic Issue for the journal Current Alzheimer Research |
Dissecting the Immunopathogenesis of Alzheimer’s Disease
Guest Editor: Prof. Yu Tang
• Scope of the Thematic Issue:
Alzheimer’s disease (AD), as the most common age-related neurodegenerative disease, is hallmarked by extensive gliosis including both microglia astrocyte activation. Glia cells play a pivotal role in mediating neuroinflammation in the central nervous system (CNS) are tightly associated with neuronal death dysfunction. Upon different stimuli, glia cells possess various phenotypes that may produce different effects on neuron functions. So far, phenotypic changes of glia cells (M1/M2 microglia, or A1/A2 astrocytes), as well as their potential effects have been increasingly investigated. Notably, with the emerging single-cell RNA-Seq technique, more more unique glial phenotypes, such as disease-associated microglia (DAM) subtype, have been revealed. Meanwhile, novel glia markers like Sall1 Tmem119 have also been increasingly identified, which would greatly expour understandings of those immune cells. Overall, it appears that glia mediated neuroinflammation is more likely to be heterogeneous, especially in the immunopathogenesis of AD. The phenotypic changes of glia are rapid rather dynamic, depending on the milieu of CNS at different disease stages, which may also greatly confound our endeavors on dissecting their functions. Moreover, increasing components, including gut microbiota aging, have been recently added to be strongly linked with neuroinflammation, thereby contributing to the development of AD.
In this special issue, we are collecting a series of comprehensive reviews on multiple aspects of the immunopathogenesis of AD. Specifically, we are interested in manuscripts that will (1) review the various functions of glial subtypes in AD; (2) summarize the discovery of novel glia phenotypes or markers by high-throughput detections, for instance, by single-cell RNA-Seq bioinformatics analysis; (3) describe the potential effects of gut microbiota that may exacerbate the AD pathogenesis; also (4) review the possible detrimental effects of aging, a major risk factor for the late-onset disease such as AD. However, any other aspects or new insights related with neuroinflammation in AD pathogenesis are encouraged to submit.
Keywords: Alzheimer’s Disease; Neuroinflammation; Microglia; Astrocyte; Phenotypic Change; Neuroprotection; Aging; Microbiota
The sub-topics to be covered within the issue should be provided:
Microglial phenotypic changes
Astrocyte phenotypic changes
Novel glia markers subtypes
Single-cell sequencing & Neuroinflammation
Pathological mutations & Neuroinflammation
Aging & Neuroinflammation
Gut microbiota & Neuroinflammation
Guest Editor: Yu Tang
Affiliation: National Clinical Research Center for Geriatric Disorders, Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, China
Email:tangyu-sky@163.com
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