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: | Jagan Pillai |
| Institution: | Cleveland Clinic Lerner College of Medicine |
| Department: | Medicine |
| Country: | |
| Proposed Analysis: | Accumulating evidence implicates inflammatory changes in AD (Wyss-Coray, 2006, Hotzman et al, 2012, Bettcher et al, 2014). The role of systemic inflammation and occurrence of amyloid plaque-dependent inflammation have been well documented in both human autopsy specimens and animal models (Perry et al, 2007, Holmes et al, 2007). In spite of the recognition of the role for neuroinflammation in the pathophysiology of AD, there are some key outstanding questions. a) Among most prior studies of inflammatory changes in AD patients, small number of inflammatory analytes were measured, typically 1-10 analytes (Song et al, 2009, Swardfager et al, 2010, Westin et al, 2012, Hye et al, 2014, Saleem et al, 2015, Lai et al, 2017). This has limited their utility to understand the specific inflammatory pathways in the CNS that might be most activated in AD and to better evaluate if they are potentially beneficial or detrimental to clinical outcomes. To help identify inflammatory pathways or networks of inflammatory analytes pertinent to AD, it is essential to develop approaches that evaluate multiple analytes concomitantly and interrogate their biological significance when expressed together, b) prior studies have predominantly focused on the peripheral compartment and it remains unclear how the inflammatory changes in the CNS relates to changes in the peripheral compartment for a large set of inflammatory molecules. This knowledge is critical to a mechanistic understanding of the pathophysiological changes related to inflammation in the peripheral and CNS compartments simultaneously and to potentially evaluate the utility of monitoring these inflammatory changes in AD for clinical outcomes. We therefore plan to determine if specific inflammatory analytes that best correlate to AD biomarkers involve known inflammatory pathway responses and whether they are concomitantly noted in both the CNS compartment (CSF) and the peripheral compartment (plasma) among mild cognitive impairment (MCI) clinical patients. After evaluation of in our institutional discovery cohort we plan to corroborate the results among MCI patients in the Alzheimer’sDisease Neuroimaging Initiative (ADNI) cohort using the same validated RBM Multi-Analyte Profile (MAP) platform from Myriad Genetics used in both cohorts.Using functional network enrichment analysis we determined the biological pathways most likely related to the inflammatory analytes and genes of significance and its potential convergence across multiple datasets of brain, CSF and plasma in the presence of markers of AD pathology.Using functional network enrichment analysis we will determine the biological pathways most likely related to the inflammatory analytes and genes of significance and its potential convergence across multiple datasets of CSF and plasma in the presence of markers of AD pathology. |
| Additional Investigators |
