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| First Name: | Gary | | Last Name: | Wenk | | Title: | Professor | | Advanced Degrees: | PhD | | Affiliation: | University of Arizona | | Department: | Neural Systems, Memory & Aging | | Street Address 1: | 350 Life Sciences North | | City: | Tucson | | State/Province: | AZ | | Zip/Postal Code: | 85724 | Country/Territory: | U.S.A. | | Phone: | 520-626-2617 | | Fax: | 520626-2618 | | Email Address: |  |
Disclosure:
(view policy)
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Member reports no financial or other potential conflicts of interest. [Last Modified: 1 October 2003]
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View all comments by Gary Wenk
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Animal Models, Neurobiology, Neuropathology, Neurotransmission, DNA microarrays, Molecular and Cell biology, Neuroimmunology, Chemistry/Pharmacology, Oxidative Stress, Drug screening
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- Chair, Clinical Neuroscience and Disease Study Section, National Institutes of Health, Washington, D.C.
- Gerontology Graduate Interdisciplinary Program Faculty, University of Arizona, Tucson, Arizona.
- Research Committee for the Arizona Center on Aging, Center of Excellence,
Arizona Health Sciences Center
- Professor, Departments of Psychology and Neurology, University of Arizona
- Research Scientist in Arizona Research Laboratories, Division of Neural Systems, Memory & Aging.
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1) A recognition of whether we're dealing with more than one disease entity or process.
2) The initiating factor in the process. As technology improves, my impression is that we'll see changes earlier and earlier in vulnerable people. How far back can we go? |
I would like to see the genome completely sequenced and deciphered. We need this to rule out some additional factors.
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Chronic, widespread neuroinflammation does not cause AD but does sculpt the pathology. A mutant, inherited gene might initiate the process but is not sufficient to maintain it in all individuals.
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Confirmation that there are no other genes that paly any role in AD. This will require an absolute knowledge of the human genome.
The actual biological role for APP. |
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