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Brain glucose metabolism in Lewy body dementia: implications for diagnostic criteria.


Maximus Peto’s Commentary

I have reported previously on studies about glucose metabolism in Alzheimer’s disease. This research group reported on their investigation of using [18F]FDG-PET to diagnose dementia with Lewy bodies and to discriminate it from Alzheimer’s and Parkinson’s diseases. The results look interesting; based on where the glucose hypometabolism is observed in the brain, “hypometabolism maps yielded extremely high discriminative power, distinguishing DLB from ADD and PD conditions with an accuracy of > 90%.” Do we know exactly why glucose metabolism declines in these various regions in the brains of people with neurodegenerative disorders? Is it as simple as loss of (metabolically active) tissue?


Brain glucose metabolism in Lewy body dementia: implications for diagnostic criteria.
Alzheimers Res Ther. 2019 Feb 23;11(1):20.
Caminiti SP, Sala A, Iaccarino L, Beretta L, Pilotto A, Gianolli L, Iannaccone S, Magnani G, Padovani A, Ferini-Strambi L, Perani D
DOI: 10.1186/s13195-019-0473-4
PubMed publication date (edat): 2/25/2019

Abstract

BACKGROUND:
[18F]FDG-PET hypometabolism patterns are indicative of different neurodegenerative conditions, even from the earliest disease phase. This makes [18F]FDG-PET a valuable tool in the diagnostic workup of neurodegenerative diseases. The utility of [18F]FDG-PET in dementia with Lewy bodies (DLB) needs further validation by considering large samples of patients and disease comparisons and applying state-of-the-art statistical methods. Here, we aimed to provide an extensive validation of the [18F]FDG-PET metabolic signatures in supporting DLB diagnosis near the first clinical assessment, which is characterized by high diagnostic uncertainty, at the single-subject level.

METHODS:
In this retrospective study, we included N = 72 patients with heterogeneous clinical classification at entry (mild cognitive impairment, atypical parkinsonisms, possible DLB, probable DLB, and other dementias) and an established diagnosis of DLB at a later follow-up. We generated patterns of [18F]FDG-PET hypometabolism in single cases by using a validated voxel-wise analysis (p < 0.05, FWE-corrected). The hypometabolism patterns were independently classified by expert raters blinded to any clinical information. The final clinical diagnosis at follow-up (2.94 ± 1.39 [0.34-6.04] years) was considered as the diagnostic reference and compared with clinical classification at entry and with [18F]FDG-PET classification alone. In addition, we calculated the diagnostic accuracy of [18F]FDG-PET maps in the differential diagnosis of DLB with Alzheimer's disease dementia (ADD) (N = 60) and Parkinson's disease (PD) (N = 36). RESULTS: The single-subject [18F]FDG-PET hypometabolism pattern, showing temporo-parietal and occipital involvement, was highly consistent across DLB cases. Clinical classification at entry produced several misclassifications with an agreement of only 61.1% with the diagnostic reference. On the contrary, [18F]FDG-PET hypometabolism maps alone accurately predicted diagnosis of DLB at follow-up (88.9%). The high power of the [18F]FDG-PET hypometabolism signature in predicting the final clinical diagnosis allowed a ≈ 50% increase in accuracy compared to the first clinical assessment alone. Finally, [18F]FDG-PET hypometabolism maps yielded extremely high discriminative power, distinguishing DLB from ADD and PD conditions with an accuracy of > 90%.

CONCLUSION:
The present validation of the diagnostic and prognostic accuracy of the disease-specific brain metabolic signature in DLB at the single-subject level argues for the consideration of [18F]FDG-PET in the early phase of the DLB diagnostic flowchart. The assessment of the [18F]FDG-PET hypometabolism pattern at entry may shorten the diagnostic time, resulting in benefits for treatment options and management of patients.

PMID: 30797240
Free Full-Text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6387558/

Maximus Peto

Max Peto is a longevity researcher and founder of Long Life Labs. A biochemist by training, he studies the biochemistry of aging and longevity and has worked with research organizations such as SENS Research Foundation, Methuselah Foundation, BioAge Labs, Life Extension Foundation, and Ichor Therapeutics. His work at Long Life Labs is focused on empowering people to understand and manage the most critical factors for better health and longer life.

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