Recent studies have uncovered a number of genes that can influence the risk of developing sporadic Alzheimer's disease (AD). However, it remains unknown exactly how these genes impact the function of cells and promote disease. It is also unknown whether drugs can be developed to target these genes in a beneficial way. The UCI Alzheimer's Disease Research Center (ADRC) recently established the first AD induced pluripotent stem (iPS) cell core to provide researchers with a powerful new approach to study the relationship between genetic risk factors and AD pathogenesis in human cells. iPS cells are a specialized cell that can be produced by adding 4 key genes to human skin or blood cells. The resulting cells can then be grown indefinitely and are pluripotent, meaning they can differentiate into any cell type within the body. By producing iPS cells from patients with AD, mild cognitive impairment, and unaffected controls, scientists can study the influence of disease-associated genes on key types of human cells such as neurons, astrocytes, and microglia. One major challenge is that researchers will likely need cells derived from many individual patients to study the effects of genes in a complex disorder such as AD. The UCI ADRC iPS core therefore aims to generate lines from over 140 individual patients. These iPS cell lines will then be made widely available to AD researchers worldwide to accelerate the discovery of novel therapeutics and enhance our understanding of the complex genetic components of AD.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Specialized Center (P50)
Project #
5P50AG016573-20
Application #
9686522
Study Section
Special Emphasis Panel (ZAG1)
Project Start
Project End
Budget Start
2019-04-01
Budget End
2020-03-31
Support Year
20
Fiscal Year
2019
Total Cost
Indirect Cost
Name
University of California Irvine
Department
Type
DUNS #
046705849
City
Irvine
State
CA
Country
United States
Zip Code
92617
Najafi, Allison R; Crapser, Joshua; Jiang, Shan et al. (2018) A limited capacity for microglial repopulation in the adult brain. Glia 66:2385-2396
Barnes, Josephine; Bartlett, Jonathan W; Wolk, David A et al. (2018) Disease Course Varies According to Age and Symptom Length in Alzheimer's Disease. J Alzheimers Dis 64:631-642
Torres, Maria D; Garcia, Octavio; Tang, Cindy et al. (2018) Dendritic spine pathology and thrombospondin-1 deficits in Down syndrome. Free Radic Biol Med 114:10-14
Burke, Shanna L; Maramaldi, Peter; Cadet, Tamara et al. (2018) Decreasing hazards of Alzheimer's disease with the use of antidepressants: mitigating the risk of depression and apolipoprotein E. Int J Geriatr Psychiatry 33:200-211
Qian, Winnie; Fischer, Corinne E; Schweizer, Tom A et al. (2018) Association Between Psychosis Phenotype and APOE Genotype on the Clinical Profiles of Alzheimer's Disease. Curr Alzheimer Res 15:187-194
Largent, Emily A; Karlawish, Jason; Grill, Joshua D (2018) Study partners: essential collaborators in discovering treatments for Alzheimer's disease. Alzheimers Res Ther 10:101
Gallagher, Damien; Kiss, Alex; Lanctot, Krista et al. (2018) Depression and Risk of Alzheimer Dementia: A Longitudinal Analysis to Determine Predictors of Increased Risk among Older Adults with Depression. Am J Geriatr Psychiatry 26:819-827
Miranda, Andre M; Herman, Mathieu; Cheng, Rong et al. (2018) Excess Synaptojanin 1 Contributes to Place Cell Dysfunction and Memory Deficits in the Aging Hippocampus in Three Types of Alzheimer's Disease. Cell Rep 23:2967-2975
Haaksma, Miriam L; Calderón-Larrañaga, Amaia; Olde Rikkert, Marcel G M et al. (2018) Cognitive and functional progression in Alzheimer disease: A prediction model of latent classes. Int J Geriatr Psychiatry 33:1057-1064
Ramsey, Christine M; Gnjidic, Danijela; Agogo, George O et al. (2018) Longitudinal patterns of potentially inappropriate medication use following incident dementia diagnosis. Alzheimers Dement (N Y) 4:1-10

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