Affiliation:
1. Department of Nuclear Medicine, Faculty of Medicine, Gazi University, Ankara, Turkey
2. Department of Neurology,
Faculty of Medicine, Hacettepe University, Ankara, Turkey
Abstract
Aims:
We aimed to investigate the interaction between β-amyloid (Aβ) accumulation
and cerebral glucose metabolism, cerebral perfusion, and cerebral structural changes in the Alzheimer's
disease (AD) clinical continuum.
Background:
Utility of positron emission tomography (PET) / magnetic resonance imaging (MRI)
hybrid imaging for diagnostic categorization of the AD clinical continuum including subjective
cognitive decline (SCD), amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease
dementia (ADD) has not been fully crystallized.
Objective:
To evaluate the interaction between Aβ accumulation and cerebral glucose metabolism,
cerebral perfusion, and cerebral structural changes such as cortex thickness or cerebral white matter
disease burden and to detect the discriminative yields of these imaging modalities in the AD clinical
continuum.
Methods:
Fifty patients (20 women and 30 men; median age: 64 years) with clinical SCD (n=11),
aMCI (n=17) and ADD (n=22) underwent PET/MRI with [18F]-fluoro-D-glucose (FDG) and [18F]-
Flutemetamol in addition to cerebral blood flow (CBF) and quantitative structural imaging along
with detailed cognitive assessment.
Results:
High Aβ deposition (increased temporal [18F]-Flutemetamol standardized uptake value
ratio (SUVr) and centiloid score), low glucose metabolism (decreased temporal lobe and posterior
cingulate [18F]-FDG SUVr), low parietal CBF and right hemispheric cortical thickness were independent
predictors of low cognitive test performance.
Conclusion:
Integrated use of structural, metabolic, molecular (Aβ) and perfusion (CBF) parameters
contribute to the discrimination of SCD, aMCI, and ADD.
Publisher
Bentham Science Publishers Ltd.
Subject
Neurology (clinical),Neurology
Cited by
1 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献