tailieunhanh - báo cáo hóa học: " Interleukin-1 mediates Alzheimer and Lewy body pathologies"

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: Interleukin-1 mediates Alzheimer and Lewy body pathologies | Journal of Neuroinflammation BioMed Central Research Open Access Interleukin-1 mediates Alzheimer and Lewy body pathologies W Sue T Griffin 1 3 4 5 Ling Liu1 Yuekui Li1 Robert E Mrak2 3 and Steven W Barger1 3 4 Address Department of Geriatrics University of Arkansas for Medical Sciences Little Rock Arkansas 72205 USA 2Department of Pathology University of Arkansas for Medical Sciences Little Rock Arkansas 72205 USA 3Department of Neurobiology Developmental Sciences University of Arkansas for Medical Sciences Little Rock Arkansas 72205 USA 4Geriatric Research Education and Clinical Center Department of Veterans Affairs Medical Center Little Rock Arkansas 72205 USA and 5Mental Illness Research Education Center Department of Veterans Affairs Medical Center Little Rock Arkansas 72205 USA Email W Sue T Griffin - griffinsuet@ Ling Liu - liuling@ Yuekui Li - liyuekui@ Robert E Mrak - mrakroberte@ Steven W Barger - bargerstevenw@ Corresponding author Published 16 March 2006 Received 30 December 2005 Accepted 16 March 2006 Journal of Neuroinflammation2006 3 5 doi l742-2094-3-5 This article is available from http content 3 1 5 2006Griffin et al 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 Background Clinical and neuropathological overlap between Alzheimer s AD and Parkinson s disease PD is now well recognized. Such cases of concurrent AD and Lewy body disease AD LBD show neuropathological changes that include Lewy bodies a-synuclein aggregates neuritic amyloid plaques and neurofibrillary tangles hyperphosphorylated tau aggregates . The cooccurrence of these clinical and neuropathological changes suggests shared pathogenic mechanisms in these .