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Article type: Short Communication
Authors: Clark, Ian A.a; * | Alleva, Lisa M.a | Vissel, Bryceb
Affiliations: [a] Research School of Biology, Australian National University, Canberra, Australia | [b] Neurodegeneration Research Group, Garvan Institute, Sydney, Australia
Correspondence: [*] Correspondence to: Ian A. Clark, Research School of Biology, Building 41, Australian National University, Canberra ACT 0200, Australia. Tel.: +61 2 6125 4363; Fax.: +61 2 6125 0313; E-mail: ian.clark@anu.edu.au.
Abstract: Both tumor necrosis factor (TNF) and leptin are, independently, under investigation as the central mechanism for Alzheimer's disease. The wider literature provides every indication that both mediators are part of the same pathways thought to cause functional loss in this condition. This association, which has not been specifically addressed in the Alzheimer's disease literature, may be a useful link to expedite future study into the pathogenesis of this condition.
Keywords: Alzheimer's disease, inflammation, leptin, tumor necrosis factor
DOI: 10.3233/JAD-2011-110266
Journal: Journal of Alzheimer's Disease, vol. 26, no. 2, pp. 201-205, 2011
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