ArticleScientific reports2015
Early astrocytosis in autosomal dominant Alzheimer's disease measured in vivo by multi-tracer positron emission tomography.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.
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Who cites it
86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 144 citations in OpenAlex.
- Association between FDG- and TSPO-PET signals across human and animal studies investigating neurodegenerative conditions: a systematic review.Molecular psychiatry · 2026Pooled it
- GFAP as a Potential Biomarker for Alzheimer's Disease: A Systematic Review and Meta-Analysis.Cells · 2023Pooled it
- Twenty-four-hour blood pressure and CSF biomarkers of Alzheimer's disease and related dementias in a community cohort.GeroScience · 2026Article
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- MAO-B status in alcohol use disorder: a [Molecular psychiatry · 2026Article
- Early functional changes and plasma GFAP in Swedish families with Autosomal Dominant Alzheimer's disease mutations.Translational psychiatry · 2026Article
- Mapping Alzheimer's disease heterogeneity with molecular imaging biomarkers.European journal of clinical investigation · 2026Review
- Stage-Dependent Function of Astrocytes in Alzheimer's Disease: A Review.Neuroscience insights · 2026Review
- Quantification of monoamine oxidase B expression withEuropean journal of nuclear medicine and molecular imaging · 2026Article
- Astrocytes as Metabolic Sensors Orchestrating Energy-Driven Brain Vulnerability in Alzheimer's Disease.Journal of neurochemistry · 2025Review
- GADD45G operates as a pathological sensor orchestrating reactive gliosis and neurodegeneration.Neuron · 2025Article
- Article
- PET imaging of neuroinflammation: any credible alternatives to TSPO yet?Molecular psychiatry · 2025Review
- DYRK1A in the physiology and pathology of the neuron-astrocyte axis.Frontiers in neuroscience · 2025Review
- Neuroinflammatory Biomarkers in Alzheimer's Disease: From Pathophysiology to Clinical Implications.International journal of molecular sciences · 2024Review
- A microglia clonal inflammatory disorder in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2024Article
- A Key Mediator and Imaging Target in Alzheimer's Disease: Unlocking the Role of Reactive Astrogliosis Through MAOB.Nuclear medicine and molecular imaging · 2024Review
- Characterization of monoamine oxidase-B (MAO-B) as a biomarker of reactive astrogliosis in Alzheimer's disease and related dementias.Acta neuropathologica · 2024Article
- Alzheimer's Disease Puzzle: Delving into Pathogenesis Hypotheses.Aging and disease · 2024Review
- Multitracer Approach to Understanding the Complexity of Reactive Astrogliosis in Alzheimer's Brains.ACS chemical neuroscience · 2024Article
26 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studying autosomal dominant Alzheimer's disease (ADAD), caused by gene mutations yielding nearly complete penetrance and a distinct age of symptom onset, allows investigation of presymptomatic pathological processes that can identify a therapeutic window for disease-modifying therapies. Astrocyte activation may occur in presymptomatic Alzheimer's disease (AD) because reactive astrocytes surround β-amyloid (Aβ) plaques in autopsy brain tissue. Positron emission tomography was performed to investigate fibrillar Aβ, astrocytosis and cerebral glucose metabolism with the radiotracers (11)C-Pittsburgh compound-B (PIB), (11)C-deuterium-L-deprenyl (DED) and (18)F-fluorodeoxyglucose (FDG) respectively in presymptomatic and symptomatic ADAD participants (n = 21), patients with mild cognitive impairment (n = 11) and sporadic AD (n = 7). Multivariate analysis using the combined data from all radiotracers clearly separated the different groups along the first and second principal components according to increased PIB retention/decreased FDG uptake (component 1) and increased DED binding (component 2). Presymptomatic ADAD mutation carriers showed significantly higher PIB retention than non-carriers in all brain regions except the hippocampus. DED binding was highest in presymptomatic ADAD mutation carriers. This suggests that non-fibrillar Aβ or early stage plaque depostion might interact with inflammatory responses indicating astrocytosis as an early contributory driving force in AD pathology. The novelty of this finding will be investigated in longitudinal follow-up studies.
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