Purpose: The value of imaging regional glucose metabolism with [F]FDG PET for the prediction of progression from mild cognitive impairment (MCI) to Alzheimer's dementia (AD) is controversial. The predictive value of imaging with [F]FDG PET was therefore tested and compared with that of imaging beta-amyloid load with [C]PIB PET in the same memory clinic population of MCI patients.
Methods: Thirty-nine patients with MCI who had undergone [F]FDG as well as [C]PIB PET were identified from a single-centre clinical registry. [F]FDG and [C]PIB PET images were rated as positive or negative for the presence of regional hypometabolism typical of AD and beta-amyloid deposition, respectively. Raters were blinded to the clinical information. Patients were followed clinically for 2.7 ± 1.2 years after PET. Cox proportional hazards models, adjusted for age and sex, were used to test the predictive value of [F]FDG PET, [C]PIB PET, and both in combination.
Results: [F]FDG PET did not significantly predict conversion to AD (p > 0.1). By contrast, models including [C]PIB PET only (p < 0.05) or both [F]FDG and [C]PIB PET (p < 0.05) significantly predicted conversion to AD. The hazard ratio for AD in patients with a positive [C]PIB scan was 10.2 (95% confidence interval 1.3-78.1). The results were confirmed by analysis of semiquantitative measures using normalized [F]FDG uptake and [C]PIB standardized uptake value ratios in AD-typical regions as continuous predictors.
Conclusion: In contrast to [C]PIB PET, [F]FDG PET did not predict conversion from MCI to AD in this clinical patient sample. Therefore, amyloid PET should be preferred for individual prediction and patient counselling in clinical practice.
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http://dx.doi.org/10.1007/s00259-018-3983-6 | DOI Listing |
Neurology
February 2025
Departments of Child Neurology and General Practice, University of Turku and Turku University Hospital, Finland.
Background And Objectives: Previous research has demonstrated increased brain amyloid plaque load in individuals with childhood-onset epilepsy in late middle age. However, the trajectory of this process is not yet known. The aim of this study was to determine whether individuals with a history of childhood-onset epilepsy show progressive brain aging in amyloid accumulation in late adulthood (Turku Adult Childhood-Onset Epilepsy study, TACOE).
View Article and Find Full Text PDFNeurol Genet
February 2025
Memory Center, Keio University School of Medicine, Tokyo, Japan.
Background And Objectives: A previous postmortem study of men with Christianson syndrome, a disorder caused by loss-of-function mutations in the gene , reported a mechanistic link between pathologic tau accumulation and progressive symptoms such as cerebellar atrophy and cognitive decline. This study aimed to characterize the relationships between neuropathologic manifestations and tau accumulation in heterozygous women with mutation.
Methods: We conducted a multimodal neuroimaging and plasma biomarker study on 3 middle-aged heterozygous women with mutations (proband 1: mid-50s; proband 2: early 50s; proband 3: mid-40s) presenting with progressive extrapyramidal symptoms.
Mult Scler Relat Disord
December 2024
Laboratory of Nuclear Medicine (LIM43), Department of Radiology and Oncology, Faculdade de Medicina-FMUSP, Universidade de São Paulo, São Paulo 05403-911, SP, Brazil. Electronic address:
Background: Multiple sclerosis (MS) is divided into Relapsing-Remitting (RRMS) and Progressive (PMS) phenotypes, both associated with spinal cord (SC) damage. MS-related disability and SC atrophy are not yet fully understood and can differ across phenotypes. A combined approach using Positron Emission Tomography (PET) and Magnetic Resonance Imaging (MRI) could provide a broader understanding of myelin changes in the cervical SC (CSC) in different MS phenotypes and the associations with disability.
View Article and Find Full Text PDFRev Esp Med Nucl Imagen Mol (Engl Ed)
December 2024
Servicio de Medicina Nuclear, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, Grupo de Imagen Molecular (IDIVAL), Santander, Spain.
Introduction: Adults with Down syndrome demonstrate striatum-first amyloid accumulation with [C]PiB PET imaging, which has not been replicated with [F]florbetapir (FBP). Early striatal accumulation has not been temporally quantified with respect to global cortical measures.
Methods: Longitudinal PiB (n=175 participants) and FBP (n=92 participants) data from the Alzheimer Biomarkers Consortium-Down Syndrome were used to measure cortical and striatal binding.
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