The chief function of the Neuropathology Core (NC) is to provide state of the art diagnostic services, to set up and maintain a collection of optimally prepared brain samples, and to supply samples for cutting edge research to investigators of the Center, affiliated Centers, and to outside neuroscientists conducting research into neurodegenerative diseases. Because humans are the only known species to naturally develop Alzheimer disease (AD) or related illnesses, the availability of carefully prepared postmortem samples is essential despite the existence of valuable transgenic animal models. Thus, human tissue-dependent studies require that the diagnostic categorization of samples of interest is as accurate as possible. This tissue must be made available quickly following the receipt of a request to enhance laboratory efficiency and productivities. Therefore, the specific aims of NC are: 1. To establish an accurate diagnosis on all brains obtained for the Center including clinico-pathological interpretations of the findings, which are recorded within two standardized reports;a) a text-based for clinicians and medical files, and b) a quantification-based report. The quantification-based report provides data to the Clinical Care / Data Management, and to the National Alzheimer's Coordinating Committee (NACC) in compliance with National Institute on Aging (NIA) requirements. Furthermore, it is used for identifying the samples in storage with variables matching those specified by requestors;2. To obtain brain samples for tissue-dependent fresh frozen studies with or without requirement of cellular morphology preservation, which are ready for immediate disbursement once categorized;and formalin fixed samples;3. To organize the collection of samples, maintain it safely, and select among the samples in storage the ones that best match the requirement of a specific study with subsequent distribution within five working days from the time the receipt of the request;4. To teach clinicians, trainees, and neuroscientists the neuropathology of the dementias, and to assist in correlating findings made in transgenic animal models with those usually occurring in the human brains;and 5. To cooperate with other Centers including the National Institute of Neurological Disorders and Stroke (NINDS) supported Udall Center.

Public Health Relevance

Defining the changes underlying dementias is prerequisite for knowing how to prevent them. Therefore, brains of individuals who died at different stage of the dementia, and recording the type, extend, and distribution of the changes must be achieved to optimize the specificity of samples defined for basic research including tissue-dependent investigations aiming at disclosing the causes of dementias.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Specialized Center (P50)
Project #
5P50AG008702-24
Application #
8574146
Study Section
Special Emphasis Panel (ZAG1-ZIJ-4)
Project Start
Project End
Budget Start
2013-06-01
Budget End
2014-05-31
Support Year
24
Fiscal Year
2013
Total Cost
$206,867
Indirect Cost
$77,592
Name
Columbia University (N.Y.)
Department
Type
DUNS #
621889815
City
New York
State
NY
Country
United States
Zip Code
10032
Besser, Lilah M; Alosco, Michael L; Ramirez Gomez, Liliana et al. (2016) Late-Life Vascular Risk Factors and Alzheimer Disease Neuropathology in Individuals with Normal Cognition. J Neuropathol Exp Neurol 75:955-962
Burke, Shanna L; Maramaldi, Peter; Cadet, Tamara et al. (2016) Neuropsychiatric symptoms and Apolipoprotein E: Associations with eventual Alzheimer's disease development. Arch Gerontol Geriatr 65:231-8
John, Samantha E; Gurnani, Ashita S; Bussell, Cara et al. (2016) The effectiveness and unique contribution of neuropsychological tests and the δ latent phenotype in the differential diagnosis of dementia in the uniform data set. Neuropsychology 30:946-960
Hur, Jang Ho; Park, Shi-Young; Dall'Armi, Claudia et al. (2016) Phospholipase D1 deficiency in mice causes nonalcoholic fatty liver disease via an autophagy defect. Sci Rep 6:39170
Bonham, Luke W; Geier, Ethan G; Fan, Chun C et al. (2016) Age-dependent effects of APOE ε4 in preclinical Alzheimer's disease. Ann Clin Transl Neurol 3:668-77
Ting, Simon Kang Seng; Hao, Ying; Chia, Pei Shi et al. (2016) Clinicopathological correlation of psychosis and brain vascular changes in Alzheimer's disease. Sci Rep 6:20858
Fischer, Corinne E; Qian, Winnie; Schweizer, Tom A et al. (2016) Lewy Bodies, Vascular Risk Factors, and Subcortical Arteriosclerotic Leukoencephalopathy, but not Alzheimer Pathology, are Associated with Development of Psychosis in Alzheimer's Disease. J Alzheimers Dis 50:283-95
Karch, Celeste M; Ezerskiy, Lubov A; Bertelsen, Sarah et al. (2016) Alzheimer's Disease Risk Polymorphisms Regulate Gene Expression in the ZCWPW1 and the CELF1 Loci. PLoS One 11:e0148717
McCutcheon, Sarah T; Han, Dingfen; Troncoso, Juan et al. (2016) Clinicopathological correlates of depression in early Alzheimer's disease in the NACC. Int J Geriatr Psychiatry 31:1301-1311
Ebbert, Mark T W; Boehme, Kevin L; Wadsworth, Mark E et al. (2016) Interaction between variants in CLU and MS4A4E modulates Alzheimer's disease risk. Alzheimers Dement 12:121-9

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