báo cáo hóa học: " Vascular consequences of passive Aβ immunization for Alzheimer's disease. Is avoidance of "malactivation" of microglia enough?"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Vascular consequences of passive Aβ immunization for Alzheimer's disease. Is avoidance of "malactivation" of microglia enough? | Journal of Neuroinflammation BioMed Central Commentary Open Access Vascular consequences of passive Ap immunization for Alzheimer s disease. Is avoidance of malactivation of microglia enough Steven W Barger 2 3 Address Department of Geriatrics University of Arkansas for Medical Sciences Little Rock Arkansas 72205 USA 2Department of Neurobiology Developmental Sciences University of Arkansas for Medical Sciences Little Rock Arkansas 72205 USA and 3Geriatric Research Education and Clinical Center Central Arkansas Veterans Healthcare System Little Rock Arkansas 72205 USA Email Steven W Barger - bargerstevenw@ Corresponding author Published II January 2005 Received 03 January 2005 Journal ofNeuroinflammation 2005 2 2 doi 1742-2094-2-2 Accepted 1 1 January 2005 This article is available from http content 2 I 2 2005 Barger licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract The role of inflammation in Alzheimer s disease AD has been controversial since its first consideration. As with most instances of neuroinflammation the possibility must be considered that activation of glia and cytokine networks in AD arises merely as a reaction to neurodegeneration. Active healthy neurons produce signals that suppress inflammatory events and dying neurons activate phagocytic responses in microglia at the very least. But simultaneous with the arrival of a more complex view of microglia evidence that inflammation plays a causal or exacerbating role in AD etiology has been boosted by genetic physiological and epidemiological studies. In the end it may be that the semantics of inflammation and glial activation must be regarded as too simplistic for the advancement of our understanding in this .

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