In vivo evidence for pre‐symptomatic neuroinflammation in a MAPT mutation carrier
Open accessAbstract
Neuroinflammation occurs in frontotemporal dementia, however its timing relative to protein aggregation and neuronal loss is unknown. Using positron emission tomography and magnetic resonance imaging to quantify these processes in a pre‐symptomatic carrier of the 10 + 16 MAPT mutation, we show microglial activation in frontotemporal regions, despite a lack of protein aggregation or atrophy in these areas. The distribution of microglial activation better discriminated the carrier from controls than did protein aggregation at this pre‐symptomatic disease stage. Our findings suggest an early role for microglial activation in frontotemporal dementia. Longitudinal studies are needed to explore the causality of this pathophysiological association.
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The presymptomatic dissociation of 11C-PK-11195 and 18F-AV-1451 binding argues strongly against simple cross-affinity.
“Moreover, the presymptomatic dissociation of 11C-PK-11195 and 18F-AV-1451 binding (Bevan-Jones et al., 2019) argues strongly against simple cross-affinity.”
From Neuroinflammation and protein aggregation co-localize across the frontotemporal dementia spectrum (2020) · cites this paper as Bevan-Jones et al., 2019
A previous report of a MAPT mutation carrier described high [11C]PK11195 binding without significant [18F]AV-1451 binding, suggesting the two ligands are not equivalent in their binding.
“However, a previous report of a carrier of a MAPT genetic mutation described high [11C]PK11195 binding in the absence of significant [18F]AV-1451 binding36, which suggests that despite the potential for a common target, the two ligands are not equivalent in their binding.”
From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [36]
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- Authors
- Bevan‐Jones, W. R., Cope, T. E., Jones, P. S., Passamonti, L., Hong, Y. T., Fryer, T., Arnold, R., Coles, J. P., Aigbirhio, F. I., O'Brien, J. T., & Rowe, J. B.
- Affiliations
- Department of Psychiatry University of Cambridge Cambridge United Kingdom
- University of Cambridge (GB)
- MRC Cognition and Brain Sciences Unit (GB)
- ORCID
- Venue
- Annals of Clinical and Translational Neurology
- Publisher
- Wiley
- Published
- 2019-01-02
- Volume
- 6
- Issue
- 2
- Pages
- 373-378
- ISSN
- 2328-9503 (ISSN-L)
- PMC
- PMC6389753
- OpenAlex
- W2907433922
- Cited by
- 36
- References
- 30
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 4 · 2023: 6 · 2022: 1 · 2021: 6 · 2020: 11 · 2019: 2 · 2018: 1
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Annals of Clinical and Translational Neurology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Apollo (University of Cambridge) (submittedVersion, cc-by)
- Apollo (cc-by)
- Funders
- National Institute for Health Research
- Wellcome Trust (103838)
- Patrick Berthoud Charitable Trust
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- frontotemporal dementia, MAPT mutations, microglial activation, tau aggregation, mutation carriers, positron emission tomography, magnetic resonance imaging
- MeSH terms
- Atrophy, Brain, Female, Heterozygote, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Middle Aged, Mutation, tau Proteins, Positron-Emission Tomography, Frontotemporal Dementia
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