The Clinical Core will continue to provide a registry of well characterized patients and control subjects to foster clinical and basic scientific research on Alzheimer's disease (AD). To capitalize on the unique strengths and research interests of Emory investigators, the following major cohorts of patients will be recruited and followed: (1) probable AD; (2) Parkinson's disease (PD) without dementia; (3) PD with dementia (PDD); and (4) control subjects without evidence of cognitive or motor impairment. African-American subjects will continue to be recruited through our Satellite Clinic and other sites, maintaining 30% participation in each of our registry cohorts, in parallel with the proportion of African-Americans in our community. Blood will be obtained on patients and control subjects for characterization of mitochondrial DNA, apolipoprotein E genotyping, and other analyses as well as the establishment of lymphoblastoid cell lines by the Molecular Core. Comprehensive and standard neurological and neuropsychological assessment designed to evaluate multiple cognitive and behavioral domains will be performed along with clinical evaluation and quantitative neurophysiological tests of motor function. These data, in combination with molecular and eventual neuropathological information will be a valuable resource for the multidisciplinary group of Emory investigators exploring the heterogeneity of AD, PD, and the overlap among these and other neurodegenerative disorders.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Center Core Grants (P30)
Project #
5P30AG010130-08
Application #
6267525
Study Section
Project Start
1998-07-01
Project End
1999-06-30
Budget Start
1997-10-01
Budget End
1998-09-30
Support Year
8
Fiscal Year
1998
Total Cost
Indirect Cost
Name
Emory University
Department
Type
DUNS #
042250712
City
Atlanta
State
GA
Country
United States
Zip Code
30322
Goldstein, Felicia C; Levey, Allan I; Steenland, N Kyle (2013) High blood pressure and cognitive decline in mild cognitive impairment. J Am Geriatr Soc 61:67-73
Procaccio, Vincent; Salazar, Gloria; Ono, Shoichiro et al. (2006) A mutation of beta -actin that alters depolymerization dynamics is associated with autosomal dominant developmental malformations, deafness, and dystonia. Am J Hum Genet 78:947-60
Goldstein, F C; Ashley, A V; Freedman, L J et al. (2005) Hypertension and cognitive performance in African Americans with Alzheimer disease. Neurology 64:899-901
Choi, Joungil; Levey, Allan I; Weintraub, Susan T et al. (2004) Oxidative modifications and down-regulation of ubiquitin carboxyl-terminal hydrolase L1 associated with idiopathic Parkinson's and Alzheimer's diseases. J Biol Chem 279:13256-64
Weiner, David M; Goodman, Matilda W; Colpitts, Tonya M et al. (2004) Functional screening of drug target genes: m1 muscarinic acetylcholine receptor phenotypes in degenerative dementias. Am J Pharmacogenomics 4:119-28
Cairns, Nigel J; Zhukareva, Victoria; Uryu, Kunihiro et al. (2004) alpha-internexin is present in the pathological inclusions of neuronal intermediate filament inclusion disease. Am J Pathol 164:2153-61
Scherzer, Clemens R; Offe, Katrin; Gearing, Marla et al. (2004) Loss of apolipoprotein E receptor LR11 in Alzheimer disease. Arch Neurol 61:1200-5
Cairns, Nigel J; Uryu, Kunihiro; Bigio, Eileen H et al. (2004) alpha-Internexin aggregates are abundant in neuronal intermediate filament inclusion disease (NIFID) but rare in other neurodegenerative diseases. Acta Neuropathol (Berl) 108:213-23
Cairns, N J; Grossman, M; Arnold, S E et al. (2004) Clinical and neuropathologic variation in neuronal intermediate filament inclusion disease. Neurology 63:1376-84
Gearing, Marla; Juncos, Jorge L; Procaccio, Vincent et al. (2002) Aggregation of actin and cofilin in identical twins with juvenile-onset dystonia. Ann Neurol 52:465-76

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