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Proper Citation: Indiana Alzheimer Disease Center (RRID:SCR_012811)
Description: The mission of the Indiana Alzheimer Disease Center is to serve as a shared research resource in order to facilitate research in Alzheimer disease and related disorders and to distinguish them from normal aging. Within this mission, one objective is to provide an environment and core resources to enhance ongoing research and foster new lines by bringing together basic and clinical scientists to study the etiology, pathogenesis, diagnosis, and treatment of Alzheimer disease and related dementias, with an emphasis on hereditary dementias. The Center is composed of 6 cores: Administrative, Clinical, Neuropathology, Data Management, Education and Information Transfer, and Imaging. The Neuropathology Core functions as brain-bank facility, which stores samples from hundreds of autopsied cases and supplies them to research investigators around the world. The focus of the IADC is on behavioral neurology, clinicopathological correlations, biochemistry, and genetics of AD, frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), Gerstmann-Str��������ussler-Scheinker disease (GSS), Parkinson disease and other hereditary diseases associated with abnormal protein accumulation. The Neuropathology Core carries out state-of-the-art neuropathological examination of brain, spinal cord and other tissue samples obtained from individuals affected by neurodegenerative dementia and/or other related neurodegenerative diseases. The Core is composed of five different laboratories: histology and immunohistochemistry, electron microscopy, molecular biology, biochemistry, as well as a small-animal laboratory dedicated to the study of murine models of human diseases. In the past 15 years, we have been among the first to discover mutations in genes implicated in the etiology and pathogenesis of early-onset dementia. Specifically we have identified novel mutations in the Amyloid Precursor Protein gene (APP) and Presenilin 1 (PSEN1) that are responsible for hereditary forms of early-onset AD. We have also found several novel mutations responsible for Gerstmann-Str��������ussler-Scheinker (GSS) disease, a hereditary degenerative disease causing ataxia, parkinsonism and dementia secondary to the accumulation of mutated prion protein (PrP). We have reported mutations in the MAPT gene in FTDP-17, a tauopathy which causes personality changes, cognitive dysfunction, rigidity and dementia. Other areas of research in neurodegeneration are related to the study of genetic mutations of Neuroserpin (SCNA) and Light Ferritin Polypeptide genes.
Abbreviations: IADC
Resource Type: tissue bank, material resource, brain bank, biomaterial supply resource
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