Premium
P4‐347: Imaging Neuroinflammation in Amnestic Mild Cognitive Impairment (AMCI) Using a Novel PET Radioligand: [18F]‐FEPPA
Author(s) -
Knezevic Dunja,
Verhoeff Nicolaas Paul L.G.,
Hafizi Sina,
Graff-Guerrero Ariel,
Mulsant Benoit H.,
Voineskos Aristotle N.,
Rajji Tarek K.,
Pollock Bruce G.,
Houle Sylvain,
Rusjan Pablo M.,
Mizrahi Romina
Publication year - 2016
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.2016.07.091
Subject(s) - translocator protein , neuroinflammation , radioligand , neuroscience , pittsburgh compound b , cognitive impairment , hippocampus , medicine , psychology , magnetic resonance imaging , pathology , cognition , disease , receptor , radiology
and SMC subjects with Am+ PETwere Tau PET+ with Braak stagelike progression. Most Tausubjects were negative for a FDG CV1 pattern. Compared to Am-Tausubjects, Tau+ subjects expressed a taupattern highly similar toADhypometabolism (FDGCV1pattern), differing in sensorimotor cortex (Figure 2). In Tau+ subjects, greater FDGCV1+pattern expressionwas associatedwith greater deposition in FDGCV1 regions (Figure 3). Twoof threeAm+Tau+ subjectswho were FDG CV1had atypical, asymmetric tau patterns or relatively minimal tau burden and showed corresponding atypical hypometabolism (Figure 4). Conclusions: Regional glucose metabolism decline is associated with tau deposition in this preliminary data set, consistent with other findings (Ossenkoppele, 2016). Typical vs. atypical tau patterns and their extent may help to explain the correlation between FDG CV1 and subsequent rate of clinical decline, and to understand whether cognitive decline arises from tau or the extent of neurodegenerative response to burden.