Premium
P2‐372: STRUCTURAL COVARIANCE NETWORKS IN AMYLOID POSITIVE PATIENTS WITH OR WITHOUT WHITE MATTER HYPERINTENSITIES
Author(s) -
Son Sang Joon,
Park Bumhee,
Roh Hyun Woong,
Youn Kyoung Sun,
Hong Chang Hyung
Publication year - 2019
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.2019.06.2779
Subject(s) - hyperintensity , white matter , thalamus , neuroscience , basal ganglia , bonferroni correction , amyloid (mycology) , magnetic resonance imaging , pathology , psychology , medicine , radiology , central nervous system , mathematics , statistics
impairment in their effect on C-PBR28 (p 1⁄4 0.6722). However, there was significant interaction between amyloid and memory status in their effect on F-MK-6240 binding (p 1⁄4 0.011). Regional effects followed a similar pattern for both radioligands (Fig 1). In amyloid-positive subjects, MMSE negatively correlated with both F-MK-6240 (p < 0.02) and C-PBR28 (p < 0.03) binding in all regions except medial temporal cortex for C-PBR28. In amyloid-negative subjects, MMSE did not correlate with binding of either radioligand in any region. Conclusions: That Ab has an effect on C-PBR28 binding in the absence of impairment suggests an early increase in microglial activation in AD, possibly prior to increased tau pathology. Similarly, that impairment has an effect on C-PBR28 binding in the absence of Ab suggests a microglial response to neurodegeneration that is not AD-specific. Negative correlation with MMSE for C-PBR28 and F-MK-6240 binding suggests both microgial activation and tau pathology increase throughout progression of disease.