Core A. Clinical examines the natural history of senile dementia of the Alzheimer type (SDAT) and healthy aging in longitudinal samples of carefully assessed subjects, using established clinical, cognitive, and neurological methods. The Core also recruits, evaluates, and supplies subjects to the individual projects in this renewal application. Clinicopathological correlations are enhanced by the Core's emphasis on obtaining autopsy permission from both nondemented and demented subjects. Data from these Core activities are compared, with the assistance of Core D. Biostatistics, with those from Core B. Psychometrics, Core C. Neuropathology, and all Projects to explore the central theme of the Program Project: the behavioral and biomedical correlates of SDAT in comparison with healthy aging. These objectives build on our previous studies in these areas. The study of very old persons (aged 80 years and over) will be expanded by enrolling additional subjects and serially assessing them until autopsy to examine areas of overlap in advanced aging and Alzheimer's disease. Core clinical data, including information obtained by a Retrospective Collateral Dementia Interview in brains obtained from the Body Donor Program or General Autopsy Service, will be correlated with detailed patho-anatomic mapping of markers of neuronal degeneration. Attentional factor affecting memory processing in aging and dementia and the effects of hypoglycemia on memory performance will be studied in Core subjects. The Core will continue to enroll subjects in the very mild stages of SDAT and follow its established samples of subjects, originally entered as controls, to distinguish the earliest clinical manifestations of disease from changes associated with aging and to identify those factors predictive of SDAT.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Program Projects (P01)
Project #
2P01AG003991-16
Application #
6097955
Study Section
Project Start
1999-01-01
Project End
1999-12-31
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
16
Fiscal Year
1999
Total Cost
Indirect Cost
Name
Washington University
Department
Type
DUNS #
062761671
City
Saint Louis
State
MO
Country
United States
Zip Code
63130
Cruchaga, Carlos; Del-Aguila, Jorge L; Saef, Benjamin et al. (2018) Polygenic risk score of sporadic late-onset Alzheimer's disease reveals a shared architecture with the familial and early-onset forms. Alzheimers Dement 14:205-214
Maxwell, Taylor J; Corcoran, Chris; Del-Aguila, Jorge L et al. (2018) Genome-wide association study for variants that modulate relationships between cerebrospinal fluid amyloid-beta 42, tau, and p-tau levels. Alzheimers Res Ther 10:86
Kinnunen, Kirsi M; Cash, David M; Poole, Teresa et al. (2018) Presymptomatic atrophy in autosomal dominant Alzheimer's disease: A serial magnetic resonance imaging study. Alzheimers Dement 14:43-53
Brainstorm Consortium (see original citation for additional authors) (2018) Analysis of shared heritability in common disorders of the brain. Science 360:
Schultz, Stephanie A; Gordon, Brian A; Mishra, Shruti et al. (2018) Widespread distribution of tauopathy in preclinical Alzheimer's disease. Neurobiol Aging 72:177-185
Ibanez, Laura; Dube, Umber; Davis, Albert A et al. (2018) Pleiotropic Effects of Variants in Dementia Genes in Parkinson Disease. Front Neurosci 12:230
Javaherian, Kavon; Newman, Brianne M; Weng, Hua et al. (2018) Examining the Complicated Relationship Between Depressive Symptoms and Cognitive Impairment in Preclinical Alzheimer Disease. Alzheimer Dis Assoc Disord :
Broce, Iris; Karch, Celeste M; Wen, Natalie et al. (2018) Correction: Immune-related genetic enrichment in frontotemporal dementia: An analysis of genome-wide association studies. PLoS Med 15:e1002504
Jansen, Willemijn J; Ossenkoppele, Rik; Tijms, Betty M et al. (2018) Association of Cerebral Amyloid-? Aggregation With Cognitive Functioning in Persons Without Dementia. JAMA Psychiatry 75:84-95
Liao, Fan; Li, Aimin; Xiong, Monica et al. (2018) Targeting of nonlipidated, aggregated apoE with antibodies inhibits amyloid accumulation. J Clin Invest 128:2144-2155

Showing the most recent 10 out of 911 publications