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P4‐084: How to follow up and cluster subjects by longitudinal changes of fibrillary amyloid imaging and CSF biomarkers? 24‐month follow up
Author(s) -
Manitsirikul Sarinporn,
Mathotaarachchi Sulantha S.,
Mohamedes Sara,
Gauthier Serge,
Beaudry Thomas,
Rosa-Neto Pedro
Publication year - 2015
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2015.06.1789
Subject(s) - voxel , amyloid (mycology) , medicine , neuroimaging , analysis of variance , psychology , biomarker , nuclear medicine , pathology , oncology , neuroscience , biology , radiology , biochemistry
P4-084 HOW TO FOLLOW UPAND CLUSTER SUBJECTS BY LONGITUDINAL CHANGES OF FIBRILLARY AMYLOID IMAGING AND CSF BIOMARKERS? 24-MONTH FOLLOW UP Sarinporn Manitsirikul, Sulantha S. Mathotaarachchi, Sara Mohamedes, Serge Gauthier, Thomas Beaudry, Pedro Rosa-Neto, McGill Centre for Studies in Aging/Translational Neuroimaging Laboratory, Montreal, QC, Canada; Bangkok General Hospital, Payathai, Thailand; McGill Centre for Studies in Aging, Montreal, QC, Canada. Contact e-mail: ju_sarinporn@yahoo.com Background: Presence of amyloid is associated with cognitive decline. Fibrillar amyloid deposition levels in brain can be detected by the increase uptake of amyloid in [F]Florbetapir(AV45)PET and decrease of csf Ab1-42. Combination of biomarkers performed better for diagnosing AD. Tau was the strongest predictor of conversion but Jack, et.al propose that CSFAb1-42 was abnormal more often than t-tau.Here,we studied the relationship between regional distributions of brain fibrillar amyloid deposition, neurodegenerative biomarkers in brain(FDG) and CSF(tau),brain structural change and cognitive function at 24-month follow-up to find the best method to follow up the subjects. Methods:We analyzed 182 participants from ADNI and try to cluster the subjects by MCLUST for R. We divided the subjects into 3 groups byCSF biomarkers andAV45 (progressive, regressive, discordant) and put threshold (2SD,1SD, Z-score) in each group. We used the baseline csf biomarkers to divide subjects into 2 subgroups (positive or negative at baseline). We compare the results from everymethod to find the best way.We also analyzed by baseline diagnosis (CN, EMCI, LMCI, AD). FDG voxel-based group comparisons were calculated with PET-SUVR resampled and blurred with a8mm Gaussian filter. Voxel-based group comparisons were calculated using RMINC. Student t tests or ANOVAwas used. Statistical tests were carried out at p<0.05. Results:We had only2cluster with MCULST.We divided subjects by csf Ab1-42and AV45 into 3 groups but when put threshold, we had only7subjects left (3progressive, 2 regressive,2 nonconcordant). Finally we used cutoff from zero. We found that subjects in regressive amyloid accumulation and CSFAb1-42 positive at baseline have lowest cognitive function at baseline. We divided subjects by another 3 methods (relation between csf Ab1-42and AVV45 with baseline tau; relation between csf tau and AV45 with baseline tau; relation between csf Ab1-42, and tau with baseline tau). For structural brain change, it was significant change in first method (relation between csf Ab1-42and AV45 with baseline csf Ab1-42) in FDG between progressive with CSFAb1-42 positive and negative at baseline. Cognitive function was significant change between progressive groupwith baseline csf tau positive and negative in LDEL (only the combination use of biomarker(fig1)). When analyzed in groupbaseonbaseline diagnosis,we found significant between progressive group in FDG in cognitive normal subjects and LDEL in EMCI subjects. Conclusions: Relation between amyloid change in csf and imaging are useful to follow up neurodegeneration. Combination of amyloid and tau biomarkers in the csf and imaging are better to follow up the cognitive function. We suggest more than 24 month-follow up to see more significant change.

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