Genomes and Genes
R Scott Turner
Affiliation: University of Michigan
- X11alpha impairs gamma- but not beta-cleavage of amyloid precursor proteinGwendalyn D King
Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48105, USA
J Neurochem 88:971-82. 2004..By specifically targeting substrate instead of enzyme X11alpha may function as a relatively specific gamma-secretase inhibitor...
- The pathology of REM sleep behavior disorder with comorbid Lewy body dementiaR S Turner
Veterans Administration Medical Center Geriatric Research Education and Clinical Center, Ann Arbor, MI 48105, USA
Neurology 55:1730-2. 2000....
- Biomarkers of Alzheimer's disease and mild cognitive impairment: are we there yet?R Scott Turner
Department of Neurology, Neuroscience Program, and Institute of Gerontology, University of Michigan, Ann Arbor, MI 48105, USA
Exp Neurol 183:7-10. 2003
- X11alpha haploinsufficiency enhances Abeta amyloid deposition in Alzheimer's disease transgenic miceInderjeet Saluja
Department of Neurology, University of Michigan, USA
Neurobiol Dis 36:162-8. 2009..The increased neuropathological indices of AD in mice expressing reduced X11alpha suggest a normal suppressor role for X11alpha on CNS Abeta/amyloid deposition...
- Synergistic effects of Munc18a and X11 proteins on amyloid precursor protein metabolismChi S Ho
Department of Physiology, Institute of Gerontology, University of Michigan Medical Center, Ann Arbor, MI 48109, USA
J Biol Chem 277:27021-8. 2002..We conclude that Munc18a acts through direct and indirect interactions with X11 proteins and powerfully regulates APP metabolism and Abeta secretion...
- The cytoplasmic adaptor protein X11alpha and extracellular matrix protein Reelin regulate ApoE receptor 2 trafficking and cell movementS Sakura Minami
Department of Neurology, Georgetown University, 4000 Reservoir Road NW, Washington, DC 20057, USA
FASEB J 24:58-69. 2010..05, n=4). In the present study, we are the first to demonstrate that ApoEr2 regulates cell movement, and both X11alpha and Reelin enhance this effect...
- Alzheimer disease pathology in cognitively healthy elderly: a genome-wide studyPatricia L Kramer
Department of Neurology, Oregon Health and Science University, Portland, OR 97239, USA
Neurobiol Aging 32:2113-22. 2011..Our findings suggest that up-regulation of reelin may be a compensatory response to tau-related or beta-amyloid stress associated with AD even prior to the onset of dementia...
- ELISA analysis of beta-secretase cleavage of the Swedish amyloid precursor protein in the secretory and endocytic pathwaysMichelle L Steinhilb
Institute of Gerontology and Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan, USA
J Neurochem 80:1019-28. 2002..These results suggest that APPsw is cleaved by beta-secretase late in the secretory pathway...
- Overexpression of hAPPswe impairs rewarded alternation and contextual fear conditioning in a transgenic mouse model of Alzheimer's diseaseKevin A Corcoran
Department of Psychology, University of Michigan, Ann Arbor, Michigan 48109, USA
Learn Mem 9:243-52. 2002..Hence, learning and memory deficits in old Tg2576 mice are limited to hippocampus-dependent tasks, despite widespread amyloid deposition in cortex, hippocampus, and amygdala...
- Idiopathic rapid eye movement sleep behavior disorder is a harbinger of dementia with Lewy bodiesR Scott Turner
Department of Neurology, University of Michigan, and Veterans Affairs Medical Center Geriatric Research Education and Clinical Center, Ann Arbor, Michigan 48105, USA
J Geriatr Psychiatry Neurol 15:195-9. 2002..Inclusion of historical or concurrent idiopathic RBD in the diagnostic criteria for DLB may improve their sensitivity, specificity, and clinical utility...
- Inherited dementiasPeter Hedera
Department of Neurology, Vanderbilt University, Nashville, Tennesse, USA
Neurol Clin 20:779-808, vii. 2002....
- Coexisting adult polyglucosan body disease with frontotemporal lobar degeneration with transactivation response DNA-binding protein-43 (TDP-43)-positive neuronal inclusionsJill G Farmer
Memory Disorders Program, Department of Neurology, Georgetown University, Washington, DC 20057, USA
Neurocase 19:67-75. 2013..It is unclear if these distinct findings are coincidental in this individual, or if pathogenic pathways may intersect to promote these coexisting pathologies...
- Stable beta-secretase activity and presynaptic cholinergic markers during progressive central nervous system amyloidogenesis in Tg2576 miceJen Tzer Gau
Department of Medicine, Division of Geriatric Medicine, the Institute of Gerontology, University of Michigan, Ann Arbor, MI 48105, USA
Am J Pathol 160:731-8. 2002..Homeostatic APPsbetaswe levels with aging suggest that progressive amyloid deposition in brain results not from increased beta-secretase cleavage of APP but from impaired Abeta/amyloid clearance mechanisms...
- FDG-PET improves accuracy in distinguishing frontotemporal dementia and Alzheimer's diseaseNorman L Foster
Center for Alzheimer s Care, Imaging and Research and Department of Neurology, University of Utah, USA
Brain 130:2616-35. 2007..FDG-PET adds important information that appropriately increases diagnostic confidence, even among experienced dementia specialists...
- A comparison of classification methods for differentiating fronto-temporal dementia from Alzheimer's disease using FDG-PET imagingRoger Higdon
University of Washington, Seattle, USA
Stat Med 23:315-26. 2004..Methods using PLS appear to be more successful. Averaging or using VOI data may also be helpful...
- Alzheimer's diseaseR Scott Turner
Neurology Service, VA Ann Arbor Healthcare System, Michigan 48105, USA
Semin Neurol 26:499-506. 2006..Novel potential disease-modifying therapies now in preclinical research or clinical trials may be more effective in preventing or arresting the progressive dementia of AD and will provide a test of the amyloid hypothesis...