Home 

 FAQs 

 Links 

The Indiana University School of Medicine (IUSOM) has a long and distinguished track record of accomplishments in the field of neurodegenerative diseases. Interest in AD research at Indiana University can be traced back to the mid 1960s, when studies on familial AD and other adult onset dementias began in the Department of Neurology and Division of Neuropathology. These studies continued in the 1970s and 1980s. Over the past 20 years, the interest in the field has progressively grown and several investigators in the Departments of Psychiatry, Neurology, Pathology, Medicine, and Medical and Molecular Genetics have joined in the studies of AD. With this growth, new resources have become available and in 1991, the IADC was funded by the National Institute on Aging (NIA). In 1993, the IADC was strengthened by the addition of the National Cell Repository devoted to the collection of immortalized cells from subjects affected by familial AD and related dementias. More recently, the IADC has undergone structural changes. First, the National Cell Repository Core was separated from the IADC into a stand-alone entity funded by the NIA in 2002. In 2004, the IADC competitively applied for and received funding for a Data Management and Statistics Core. The data management and statistical functions that were originally in the Administrative Core are now provided by this new core. Through this competitive application, the resources available for data management and statistics have increased. The remaining cores of the center are unchanged. With the rapid changes occurring to ADCs both scientifically and structurally, it is necessary to have the flexibility to modify directions and to add new goals as needed for the IADC. This requires the interaction between the director and the NIA, executive committee, external advisory committee and National Alzheimer’s Coordinating Center (NACC).

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-Sträussler-Scheinker disease (GSS), Parkinson disease and other hereditary diseases associated with abnormal protein accumulation.

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-Sträussler-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.

Links:
- More Information