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Updated 24 September 2004
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A "Mitochondrial Cascade Hypothesis" for Sporadic Alzheimer's Disease
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Russell H. Swerdlow and Shaharyar Khan led this live discussion on 24 September 2004. Readers are invited to submit additional comments by using our Comments form at the bottom of the page.
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View Transcript of Live Discussion — Posted 22 August 2006
Background Text
The amyloid cascade hypothesis has been evoked to explain the pathology
that underlies Alzheimer disease. It claims that "deposition of Aβ,
the main component of plaques, is the causative agent of Alzheimer's
pathology, and that the neurofibrillary tangles, cell loss, vascular
damage, and dementia follow as a direct result of this deposition" (see
Hardy et al., 1992).
But what triggers deposition of Aβ—what lies upstream? Recently, in
the journal Medical Hypotheses, Russell Swerdlow and Shaharyar Khan
proposed the "mitochondrial cascade hypothesis," which attempts to tie
together seemingly disparate pathological features of the disease. Read
the full hypothesis then join us on Friday,
24 September 2004, when Russell and Shaharyar lead a Live Discussion on their
theories. We are grateful to Elsevier Ltd. for providing Alzforum with
the manuscript free of charge.—Tom Fagan
See Full Text (.pdf) of this article. Reprinted from with permission from Elsevier. Swerdlow, Russell H. and Khan, Shaharyar. A "Mitochondrial Cascade Hypothesis" for Sporadic Alzheimer's Disease. Medical Hypotheses. 2004; 63: 8-20. See ScienceDirect.
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