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: | Huimin Chen |
| Institution: | Beijing Tiantan Hospital, Capital medical university |
| Department: | Department of Neurology |
| Country: | |
| Proposed Analysis: | Background: We previously investigated the role of cerebral small vessel disease in Parkinson’s disease (PD), and found perivascular space (PVS) was only associated with cognitive impairment in PD, while other imaging markers were associated with both motor, mood and cognitive domains, in consistence with previous publication (doi: 10.1002/mds.27798). As emerging evidence has highlighted that PVS may function as a lymphatic system of central nervous system for waste clearance, we asked whether enlarged PVS seen on MRI reflected higher burden of CSF neurodegenerative biomarkers. Using another open access dataset (parkinson's progression markers initiative, PPMI), we did find significant association between PVS and CSF pTau, and between PVS and CSF tTau in PD, independent of age, white matter hyperintensity, disease duration, MoCA, and MDS-UPDRS III. However, only CSF biomarkers, but not PVS or biomarker*PVS interactions, was found to be predictive of cognitive impairment at 2-year follow up using logistic model (cognitive state as the dependent parameter) or linear regression model (change in Moca as the dependent parameter), which means PVS may reflect CSF neurodegenerative burden but may not be pathologic itself. Therefore, we intend to apply for ADNI data to confirm these findings in Alzheimer disease (AD), especially to test whether PVS is independently associated with cognitive impairment or is just an epiphenomenon. Aim: to investigate the interaction between PVS and cerebrospinal Abeta/tTau, and the role of PVS and PVS* Abeta/tTau interaction in the prognosis of AD. Method: Baseline basal ganglia and centrum semiovale PVS will be evaluated using semiquantitative scales ranging from 0 to 4, which was developed by Edinburg group. Basal ganglia and centrum semiovale PVS will be analyzed separately. For statistical analysis, firstly, patients will be divided into 2 groups according to PVS severity (Basal ganglia PVS 0-1 vs 2-4; centrum semiovale PVS 0-1 vs 2-4). Baseline and longitudinal value of Abeta/tTau will be compared between PVS groups. Repeated-measures ANOVA will also be conducted to assess the time*PVS effect. Change in Abeta/tTau from baseline to follow-ups will be calculated and used as dependent variable in linear or general linear models with adjustment for age, disease duration et.al. Then, a logistic model with cognitive state as dependent variable, with PVS, Abeta/tTau and PVS*Abeta/tTau interaction (additive and multiplied interaction) as independent variable will be conducted to explore whether PVS mediate the role of Abeta/tTau in the cognitive impairment in AD. |
| Additional Investigators |
