The overarching objective of the Massachusetts Alzheimer's Disease Research Center (MADRC) is to stimulate and support research of the highest quality in aging, Alzheimer's disease (AD), and related disorders. The specific goals are: To propose and support new research directed toward uncovering the etiology and pathogenetic mechanisms of AD and related dementias;to enhance collaborative research funded outside of the MADRC;and to catalyze education, training and information transfer related to dementia. Administrative, Clinical, Data and Statistical, Neuropathology, and Education Cores support 3 R01 style 5 year projects and 3 pilot projects/year. The Clinical Core has established a Longitudinal Cohort that follows ~600 individuals who are cognitively normal, have mild impairments, mild AD or other dementias. These subjects undergo full Uniform Data Set evaluations and data are submitted to NACC. Our retention rate to date (93% 1 year;97% 2 year) shows that these individuals are committed to participate in longitudinal studies. Over 60% of these individuals have already also contributed to at least one other research project related to aging and cognition, including 7 different neuroimaging studies and a major Biomarkers program. The Neuropathology Core has tissues on nearly 1400 subjects, and in the last 4 years supplied 3 dozen separate investigators with over 10,000 slides or specimens. The Data and Statistics Core has built a new state of the art data repository. The Education Core has continued its mission of outstanding community involvement, and has enhanced recruitment for MADRC programs. Three R01 style applications are closely linked to Core activities, and focus on the relationship between amyloid, clinical symptoms, and neurotoxicity: Two relate to longitudinal studies in MADRC subjects. The first asks what does positive PIB amyloid imaging mean in the setting of normal cognition? The second, led by a junior investigator, examines whether amyloid deposition in vessels (CAA) alters the course of dementia. The third project utilizes MADRC brain bank material to examine whether oligomeric forms of amyloid - in addition to, or instead of, fibrillar forms - are neurotoxic. The MADRC provides infrastructure to support local and national efforts in AD research: In the current grant period 44 investigators used MADRC resources to support 76 NIH funded projects;an additional 68 projects supported by non-Federal sources relied in part on MADRC for subjects or other resources. Going forward, the MADRC will continue to expand its clinical and neuropathological resources, its innovative training and scientific programs directed toward AD research.

Public Health Relevance

Alzheimer's disease is a devastating disorder of cognition causing dementia in millions of Americans. Our studies use clinical and laboratory tools to characterize the earliest phases of the disease, and to try to better understand the underlying causes of the brain damage that leads to dementia.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Specialized Center (P50)
Project #
2P50AG005134-26
Application #
7620491
Study Section
Special Emphasis Panel (ZAG1-ZIJ-4 (J1))
Program Officer
Phelps, Creighton H
Project Start
1997-04-01
Project End
2014-03-31
Budget Start
2009-05-01
Budget End
2010-03-31
Support Year
26
Fiscal Year
2009
Total Cost
$1,989,373
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
073130411
City
Boston
State
MA
Country
United States
Zip Code
02199
Rieckmann, Anna; Johnson, Keith A; Sperling, Reisa A et al. (2018) Dedifferentiation of caudate functional connectivity and striatal dopamine transporter density predict memory change in normal aging. Proc Natl Acad Sci U S A 115:10160-10165
Jacobs, Heidi I L; Hedden, Trey; Schultz, Aaron P et al. (2018) Structural tract alterations predict downstream tau accumulation in amyloid-positive older individuals. Nat Neurosci 21:424-431
Martinez-Ramirez, Sergi; van Rooden, Sanneke; Charidimou, Andreas et al. (2018) Perivascular Spaces Volume in Sporadic and Hereditary (Dutch-Type) Cerebral Amyloid Angiopathy. Stroke 49:1913-1919
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
Putcha, Deepti; McGinnis, Scott M; Brickhouse, Michael et al. (2018) Executive dysfunction contributes to verbal encoding and retrieval deficits in posterior cortical atrophy. Cortex 106:36-46
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
Mordes, Daniel A; Prudencio, Mercedes; Goodman, Lindsey D et al. (2018) Dipeptide repeat proteins activate a heat shock response found in C9ORF72-ALS/FTLD patients. Acta Neuropathol Commun 6:55
Qian, Jing; Chiou, Sy Han; Maye, Jacqueline E et al. (2018) Threshold regression to accommodate a censored covariate. Biometrics :
Makaretz, Sara J; Quimby, Megan; Collins, Jessica et al. (2018) Flortaucipir tau PET imaging in semantic variant primary progressive aphasia. J Neurol Neurosurg Psychiatry 89:1024-1031
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

Showing the most recent 10 out of 966 publications