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| First Name: | Frank | | Last Name: | Gunn-Moore | | Title: | Reader in Neuroscience | | Advanced Degrees: | BSc PhD | | Affiliation: | University of St Andrews | | Department: | Biology | | Street Address 1: | Medical and Biological Sciences Building | | Street Address 2: | North Haugh | | City: | St Andrews | | State/Province: | Fife | | Zip/Postal Code: | KY16 9TF | Country/Territory: | United Kingdom | | Phone: | 01334 463525 | | Fax: | 01334 463600 | | Email Address: |  |
Disclosure:
(view policy)
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Member reports no financial or other potential conflicts of interest. [Last Modified: 15 June 2011]
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View all comments by Frank Gunn-Moore
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Alzheimer Disease, Neurodevelopmental Disorders (Down syndrome, etc.), Aging Process
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Molecular and Cell biology, Protein structure/chemistry, Signal transduction, A-beta PP/A-beta, Apoptosis/Cell cycle, Chemistry/Pharmacology, Proteomics, Neuropathology, Animal Models, Oxidative Stress, Neurobiology
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Yao J, Du H, Yan S, Fang F, Wang C, Lue L-F, Guo L, Chen D, Stern D, Gunn-Moore F, Chen J, Arancio O & Yan SD (2011) Inhibition of ABAD-A interaction reduces A accumulation and improves mitochondrial function in a mouse model of Alzheimer's disease. Journal of Neuroscience 31(6):2313-20.
Muirhead KEA, Froemming M, Li X, Musilek K, Conway SJ, Sames D & Gunn-Moore FJ (2010) (–)-CHANA, a Fluorogenic Probe for Detecting Amyloid Binding Alcohol Dehydrogenase HSD10 Activity in Living Cells. ACS Chemical Biology 5(12):1105-14
Muirhead K, Borger E, Aitken L, Conway S & Gunn-Moore FJ (2010) The consequences of intracellular beta-amyloid in Alzheimer’s disease. Biochemical Journal 426(3):255-270
Du H, Guo L, Fang F, Chen D, Sosunov A, McKhann G, Yan Y, Wang C, Zhang H, Molkentin J, Gunn-Moore FJ, Vonsattel JP, Arancio O, Chen J & Yan SD Deficiency of Cyclophilin D attenuates mitochondrial and neuronal perturbation, and ameliorates learning memory in Alzheimer’s disease (2008) Nature Medicine. 14(10) 1097-105
Ren Y, Fang F, Davey F, Taylor M, Aiton J, Coote P, Yao J, Chen JX, Yan SD & Gunn-Moore FJ. Endophilin I expression is increased in the brains of Alzheimer’s disease patients. (2008) Journal of Biological Chemistry, 283, 5685-91.
Yao Y, Taylor M, Davey F, RenY, Aiton J , Coote P, Chen X, Yan SD & Gunn-Moore FJ. Interaction of Amyloid binding Alcohol Dehydrogenase/Aβ mediates up-regulation of peroxiredoxin II in the brains of Alzheimer’s disease patients and a transgenic Alzheimer’s disease mouse model. (2007) Molecular and Cellular Neuroscience, 35, 377–82
Gunn-Moore D, McVee J, Bradshaw J, Pearson G, Head E & Gunn-Moore F -Amyloid and hyperphosphorylated tau deposition in cat brains. (2006) Journal of Feline Medicine & Surgery, 8, 234-42.
Lustbader J., Cirilli M., Lin, C., Xu HW., Takuma K., Wang N., Caspersen C., Chen X., Pollack S., Chaney M., Trinchese F., Liu S., Gunn-Moore F., Lue L-F., Walker D., Kuppusamy P., Zewier Z., Arancio O., Stern D., Yan SD. & Wu H. (2004) ABAD directly links A to mitochondrial toxicity in Alzheimer's disease. Science, 304, 448-52.
Charles P, Tait S., Faivre-Sarrailh C., Barbin G., Gunn-Moore F., Denisenko-Hehrbass N., Guennoc A-M., Girault J, Brophy P. & Lubetzki C. (2002) Neurofascin is a glial receptor for the caspr/paranodin-contactin axonal complex at the axoglial junction. Current Biology, 12, 217-20.
Powell A.J., Read J.A., Banfield M.J., Gunn-Moore F., Yan S.D., Lustbader J., Stern A.R., Stern D.M. & Brady R.L. (2000) Recognition of structurally diverse substrates by type II 3-hydroxyacyl-CoA dehydrogenase (HADH II)/amyloid-beta binding alcohol dehydrogenase (ABAD). Journal of Molecular Biology, 303(2), 311-27.
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That the intracellular production of beta amyloid has a leading contribution in the development of Alzheimer's disease. |
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