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P4‐080: Differences in saliency network between Alzheimer's and parkinson's disease
Author(s) -
Multani Namita,
Anor Cassandra Jessica,
Tang-Wai David,
Keren Ron,
Lang Anthony E.,
Fox Susan,
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.2015.06.1785
Subject(s) - psychology , personality , conscientiousness , neuroscience , dorsolateral prefrontal cortex , cognition , big five personality traits , neuroticism , resting state fmri , parkinson's disease , salience (neuroscience) , disease , prefrontal cortex , developmental psychology , cognitive psychology , medicine , extraversion and introversion , social psychology
Background: Clinical progression is individually variable among patients with Alzheimer’s disease (AD). To assess the impact of potentially disease modifying therapies on the neurodegenerative process it is essential to objectively track the progression of the underlying AD pathology. However, it is matter of debate which biomarkers are most sensitive to disease progression. Methods: In a sample of people with early clinical AD (CDR SOB 0.5-9.0) who were followed up longitudinally over an average interval of 27 months (range: 23-30 months) the progression of different imaging biomarkers of AD pathology were compared. These included amyloid deposition using [11C]PiB PET (reference tissue model: cerebrum/ cerebellar vermis SUV ratio), neuronal glucose metabolic activity using [18F]FDG PET (reference tissue model: cerebrum/ pons SUV ratio), and brain atrophy using cortical thickness (cerebrum, absolute value). Sample sizes required to detect a significant change (p<0.05) of the biomarker signal were calculated. Results: Based on real longitudinal data, post hoc power calculation revealed effect sizes for PiB, FDG, and cortical thickness of 1.299, 0.213, and 0.914, respectively. Thus, to detect statistically significant changes in future studies with a power of 80% (a 1⁄4 5%, b 1⁄4 20%) sample sizes of at least n1⁄47 for PiB, of n1⁄4176 for FDG, and of n1⁄412 for cortical thickness are required. Conclusions: Considering an imaging biomarker of AD as a surrogate for disease progression in an early AD sample, amyloid imaging with PiB or brain atrophy with cortical thickness will require relatively small sample sizes.