There are many active research projects accessing and applying shared ADNI data. Use the search above to find specific research focuses on the active ADNI investigations. This information is requested annually as a requirement for data access.
| Principal Investigator | |
| Principal Investigator's Name: | Rawan Tarawneh |
| Institution: | Cleveland Clinic |
| Department: | Ohio State University- Department of Neurology |
| Country: | |
| Proposed Analysis: | We have recently demonstrated the diagnostic and prognostic utility of the synaptic marker, neurogranin, in AD (Tarawneh et al, JAMA Neurology 2016). Our findings suggest that CSF neurogranin levels predict future cognitive decline in cognitively normal individuals (i.e. progression from CDR 0 to CDR ≥ 0.5) over a 2-3 year follow-up period, and correlate with whole brain and regional atrophy, and rates of cognitive decline in symptomatic AD. In this proposed study, I would like to investigate associations between baseline CSF neurogranin levels and i) rates of cognitive decline as indicated by annual change in psychometric scores for episodic memory, semantic memory, working memory, visuospatial functions, and global cognitive scores in longitudinal analyses of cognitively normal individuals (CDR 0) who have had at least 2 cognitive assessments, and ii) rates of whole brain or regional atrophy as indicated by rates of decline in normalized whole brain volumes, and cortical volume or thickness measures of the following regions: hippocampus, entorhinal cortex, parahippocampal gyrus, cingulate, fusiform, precuneus, and paracalcarine cortex (as a control region) in cognitively normal individuals (CDR 0) who have had at least 2 MRI assessments over the follow-up period. In these analyses, mixed linear models will be used to assess for correlations between baseline CSF neurogranin levels and rates of cognitive decline or brain atrophy over the follow-up period. Analyses will be performed for cognitively normal individuals (CDR 0) who have evidence of cortical amyloid deposition on PET-PIB (i.e. preclinical AD) and those without significant cortical amyloid deposition (i.e. PET-PIB negative) for comparison. For these analyses, I would like to request baseline clinical, demographic, APOE4 genetic data, and longitudinal psychometric and MRI volumetric data for cognitively normal individuals (CDR 0) whose CSF neurogranin data is available in the ADNI database. |
| Additional Investigators | |
| Investigator's Name: | Maciej Pietrzak |
| Proposed Analysis: | Relationship between TOMM40 and metabolomics in AD |
