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O3‐02‐04: Does Neuroinflammation Predate Amyloid Formation in Subjects at Risk for Alzheimer’s Disease?
Author(s) -
Femminella Grazia Daniela,
Dani Melanie,
Fan Zhen,
Calsolaro Valeria,
Atkinson Rebecca,
Waldman Adam,
Brooks David J.,
Edison Paul,
Wood Melanie
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.2016.06.515
Subject(s) - neuroinflammation , pathology , amyloid (mycology) , posterior cingulate , alzheimer's disease , putamen , neuroscience , medicine , psychology , cortex (anatomy) , disease
gitudinal). [F]FDG intensity was normalized to the pons. Baseline global cortical [F]Florbetapir and mean parietal [F]FDG SUVR, as well as 2yr annualized percent change (APC) in global [F]Florbetapir were extracted. Baseline and 2-year hippocampal volumes (HV) were estimated using Freesurfer v5.1. Step-wise linear models predicting cortical or MTL [F]AV-1451 SUVR with the following predictors were assessed: cortical [F]Florbetapir SUVR, annual percent change (APC) in cortical [F]Florbetapir SUVR, mean parietal [F]FDG SUVR, HV, APC in HV, diagnosis (control or MCI/AD), age, gender, and time between scans. Results:Mean cortical [F]AV-1451 uptake was predicted only by diagnosis and cross-sectional mean cortical [F]Florbetapir SUVR. However, MTL [F]AV-1451 uptake was predicted by both mean cross-sectional cortical [F]Florbetapir uptake and cross-sectional HV. Conclusions: Overall, [F]AV-1451 uptake (representative of tau deposition) was predicted by the extent of cortical amyloid deposition ([F]Florbetapir uptake) approximately three years prior. Hippocampal atrophy may interact with this process. [1] Risacher et al. (2015) Alzheimer’s & Dementia, (11): 1417.