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IC‐P‐056: Differences in saliency network between Alzheimer's and parkinson's disease
Author(s) -
Multani Namita,
Anor Cassandra Jessica,
Tang-Wai David,
Keren Ron,
Fox Susan,
Lang Anthony E.,
Marras Connie,
Tartaglia Maria Carmela
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.2015.06.077
Subject(s) - psychology , personality , neuroscience , big five personality traits , conscientiousness , dorsolateral prefrontal cortex , neuroticism , cognition , salience (neuroscience) , resting state fmri , parkinson's disease , disease , personality changes , prefrontal cortex , developmental psychology , medicine , extraversion and introversion , social psychology
Background:Gerstmann–Str€aussler–Scheinker Disease (GSS) is a familial neurodegenerative disorder associated with mutations in the prion protein (PrP) gene (PRNP). A mutation in PRNP at codon 198 (c.593T>C) results in a form of GSS (p.Phe198Ser) characterized neuropathologically by neurofibrillary tangles and PrP amyloid deposition and clinically by ataxia, extrapyramidal signs, dysarthria, and cognitive decline. Patients with valine homozygosity at amino acid position 129 of PrP have an earlier onset of disease than those who are heterozygous for methionine/valine. In this study, we assessed brain glucose metabolism using [F]Fluorodeoxyglucose (FDG) positron emission tomography (PET) on a voxel-wise basis in twelve GSS F198S mutation carriers and ten non-carriers (NC). To our knowledge, this is the largest study to investigate [F]FDG uptake in GSS subjects with the F198S mutation. Methods: Twelve GSS F198S mutation carriers and ten NCs were imaged using [F]FDG PET with standard techniques. A static 30-60 minute image was created and normalized to a pons reference region to create an SUVR image for each participant. These SUVR images were then assessed on a voxel-wise basis for the effect of clinical diagnosis and mutation carrier status. Voxel-based analyses were covaried for age and gender. Findings were displayed at a voxel-wise threshold of p<0.01 (uncorrected) and minimum cluster size (k) 1⁄4 50 voxels. SPM8 was used for all pre-processing and voxel-wise statistical analyses. Results: At the time of the scan, seven GSS F198S mutation carriers were symptomatic (SC), showing signs of motor and cognitive impairment or dementia, and five GSS F198S mutation carriers were asymptomatic (AC). All NCs showed no cognitive impairment. SCs showed lower glucose metabolism in the left striatum compared to ACs and NCs, and bilaterally in the cerebellum compared to NCs (Fig. 1A-C). ACs showed hypometabolism in the right cerebellum compared to NCs (Fig. 1D). Conclusions: These findings suggest that hypometabolism in the cerebellar and striatal regions may partially underlie motor and cognitive dysfunction in GSS F198S patients.