SynthesisHuman brain mapping2025
Spatial Dissociation of Atrophy and Hypophysiology in Alzheimer's Disease: Implications for Biomarkers.
Synthesis in Human brain mapping, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Brain Structural Abnormalities in Addiction Disorders: Transdiagnostic Meta-Analyses.Human brain mapping · 2026Pooled it
- Spatial Dissociation of Atrophy and Hypophysiology in Alzheimer's Disease: Implications for Biomarkers.Human brain mapping · 2025Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The Amyloid/Tau/Neurodegeneration (A/T/N) biomarker framework is used for in vivo pathological profiling of Alzheimer's disease. A binary (+/-) label is assigned for each pathology (A, T, N) based on its presence or absence as determined by imaging or fluid biomarkers. Using imaging, neurodegeneration is confirmed by either structural MRI (indicating atrophy) or 18F-FDG PET (indicating hypometabolism), implicitly assuming that both modalities identify equivalent pathology. Preliminary evidence suggests that atrophy and hypometabolism do not spatially co-localize and are likely caused by distinct underlying pathologies. Further, while MRI is widely available, many sites lack access to PET. Recent evidence indicates that hemodynamic indices, identified via functional MRI or SPECT, may be spatially concordant with hypometabolism identified by 18F-FDG-PET and able to serve as reliable proxies. Coordinate-based meta-analyses of voxel-based morphometry and voxel-based physiology reports in Alzheimer's disease, collectively analyzing 139 articles (4218 individuals) were performed to test the following hypotheses: (1) that atrophy and hypometabolism in AD are spatially dissociated; (2) that hemodynamic indices exhibit the same spatial distributions as hypometabolism identified by PET; (3) that regions of atrophy and hypometabolism involve different functional systems and cognitive operations. Results confirmed all three hypotheses. Separation of atrophy and hypometabolism into two distinct subcategories of neurodegeneration as well as the development of regionally specific biomarkers for each are in order.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.