Neurology Journal
May 9, 2017 vol. 88 no. 19 1814-1821
Kok Pin Ng, MRCP, Tharick A. Pascoal, MD, Sulantha Mathotaarachchi, MSc, Chang-Oh Chung, MD, Andréa L. Benedet, MSc, Monica Shin, MSc, Min Su Kang, BSc, Xiaofeng Li, MD, Maowen Ba, MD, Nagaendran Kandiah, FRCP, Pedro Rosa-Neto, MD, PhD, Serge Gauthier, MD
Abstract
Objective: To identify regional brain metabolic dysfunctions associated with neuropsychiatric symptoms (NPS) in preclinical Alzheimer disease (AD).
Methods: We stratified 115 cognitively normal individuals into preclinical AD (both amyloid and tau pathologies present), asymptomatic at risk for AD (either amyloid or tau pathology present), or healthy controls (no amyloid or tau pathology present) using [18F]florbetapir PET and CSF phosphorylated tau biomarkers. Regression and voxel-based regression models evaluated the relationships between baseline NPS measured by the Neuropsychiatric Inventory (NPI) and baseline and 2-year change in metabolism measured by [18F]fluorodeoxyglucose (FDG) PET.
Results: Individuals with preclinical AD with higher NPI scores had higher [18F]FDG uptake in the posterior cingulate cortex (PCC), ventromedial prefrontal cortex, and right anterior insula at baseline. High NPI scores predicted subsequent hypometabolism in the PCC over 2 years only in individuals with preclinical AD. Sleep/nighttime behavior disorders and irritability and lability were the components of the NPI that drove this metabolic dysfunction.
