Curr Alzheimer Res. 2023;20(7):481-495. doi: 10.2174/0115672050243131230925034334.

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.

PMID:38050727 | DOI:10.2174/0115672050243131230925034334