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| First Name: | Changiz | | Last Name: | Geula | | Title: | Professor of Neuroscience | | Advanced Degrees: | Ph.D. | | Affiliation: | Northwestern University, Feinberg School of Medicine | | Department: | Cognitive Neurology and Alzheimer's Disease Center | | Street Address 1: | 320 East Superior Street | | Street Address 2: | Searle 11-465 | | City: | Chicago | | State/Province: | IL | | Zip/Postal Code: | 60611 | Country/Territory: | U.S.A. | | Phone: | (312) 503-7210 | | Fax: | (312) 908-8789 | | Email Address: |  |
Disclosure:
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Member reports the following financial or other potential conflicts of interest: [Last Modified: 4 December 2006]
Grant recipient from Novartis Pharmaceuticals
Member of Novartis Pharmaceuticals Speaker's Bureau
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View all comments by Changiz Geula
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Alzheimer Disease, Tauopathies, Aging Process, Neuromuscular Disorders (ALS, etc.), Parkinson Disease
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A-beta PP/A-beta, Animal Models, Neuropathology, Neurotransmission, DNA microarrays, Microscopy, Neurobiology, Chemistry/Pharmacology, Oxidative Stress, Tau/Cytoskeleton
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Research institute, University, University, Hospital
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Changiz Geula, PhD, is Associate Professor, Department of Medicine (Neuroscience), at Harvard Medical School, Boston, Massachusetts. Dr. Geula is also Director of the Laboratory for Neurodegenerative and Aging Research at the Beth Israel Deaconess Medical Center, Department of Medicine, Harvard Medical School.
Dr. Geula received his doctorate in Biopsychology/Neuroscience from Wayne State University, Detroit, Michigan. Postdoctoral training includes a fellowship in Neurochemistry at the University of Kentucky Medical School, Department of Neurology and Sanders-Brown Research Center on Aging, Lexington, Kentucky. He also completed a research fellowship in Neuroanatomy and Neuropathology at Harvard Medical School, Department of Neurology, Beth Israel Hospital.
Dr. Geula’s research interests have focused on the chemical and molecular anatomy of the nervous system with special emphasis on the cholinergic system; aging of the brain and Alzheimer’s disease; mechanisms of motor neuron degeneration; and excitatory amino acid neurotransmitters. He has served as principal or co-principal investigator for numerous studies on Alzheimer’s disease, including most recently a study on primate models for testing of agents with potential to protect against Alzheimer’s amyloid toxicity and a study on calbindin and cholinergic neurons in aging and Alzheimer’s disease.
Dr. Geula is a member of the Society for Neuroscience, the International Brain Research Organization, and the American Association for the Advancement of Science. |
Wu, C.-K., Nagykery, N., Hersh, L.B., Scinto, L.F.M. and Geula, C. Selective Age-Related Loss of Calbindin-D28k from Basal Forebrain Cholinergic Neurons in the Common Marmoset (Callithrix jacchus). Neurosci., In Press.
Lauckner, J., Frey, P. and Geula, C. Comparative Distribution of Tau Phosphorylated at Ser262 in Pre-Tangles and Tangles. Neurobiol. Aging, In Press.
Bu, J., Sathyendra, V., Nagykery, N. and Geula, C. Age-Related Changes in Calbindin-D28k, Calretinin and Parvalbumin Immunoreactive Neurons in the Human Cerebral Cortex. Exp. Neurol., In Press.
Geula, C., Nagykery, N., Wu, C.-K. and Bu, J. Loss of Calbindin-D28k from Aging Human Cholinergic Basal Forebrain: Relation to Plaques and Tangles. J. Neuropathol. Exp. Neurol., In Press.
Sani, S., Klink, A., Traul, D., Niaraki, N., Wu C.-K. and Geula, C. Distribution, Progression and Chemical Composition of Cortical Amyloid-b Deposits in Aged Rhesus Monkeys: Similarities to the Human. Acta Neuropathol., 102:145-156, 2003.
Geula, C., Bu, J., Nagykery, N., Scinto, L.F.M., Chan, J.C., Joseph, J. and Wu, C.-K. Loss of Calbindin-D28K from Aging Human Cholinergic Basal Forebrain: Relation to Neuronal Loss. J. Comp. Neurol., 455:249-59, 2003.
Scinto, L.F.M., Wu, C.K., Firla, K.M., Daffner, K.R., Saroff, D. and Geula, C. Focal Pathology in the Edinger-Westphal Nucleus Explains Pupillary Hypersensitivity in Alzheimer’s Disease. ACTA Neuropathol., 97:557-564, 1999.
Geula, C., Wu, C.-K., Saroff, D., Lorenzo, A., Yuan, M. and Yankner, B.A. Aging Renders the Brain Vulnerable to Amyloid b-Protein Toxicity. Nature Medicine, 4:827-831, 1998.
Geula, C., Schatz, C.R. and Mesulam, M.-M. Differential Localization of NADPH-Diaphorase and Calbindin-D 28K Within the Cholinergic Neurons of the Basal Forebrain, Striatum and Brainstem in the Rat, Monkey, Baboon and Human. Neurosci., 54:461-476, 1993.
Geula, C. and Mesulam, M-M. Cortical Cholinergic Fibers in Aging and Alzheimer's Disease: A Morphometric Study. Neurosci., 33:469-481, 1989. |
The initiating factors which cause the disease. |
That intraneuronal accumulation of amyloid-beta and abnormally phosphorylated tau are the initial contributors to neuronal dysfunction (and perhaps loss) and cognitive impairment. |
That neuronal with intracellular accumulation of the above proteins will display abnormalities in expression of genes and proteins and in function and that these abnormalities correlate with cognitive deficits in the ealiest stages of the disease (and perhaps in mild cognitive impairment). |
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