Longitudinal influence of microglial activation and amyloid on neuronal function in Alzheimer’s disease
Abstract
Amyloid deposition, tangle formation, neuroinflammation and neuronal dysfunction are pathological processes involved in Alzheimer's disease. However, the relative role of these processes in driving disease progression is still unclear. The aim of this positron emission tomography study was to: (i) investigate longitudinal changes of microglial activation, amyloid and glucose metabolism; and (ii) assess the temporospatial relationship between these three processes in Alzheimer's disease. A group of eight patients with a diagnosis of Alzheimer's disease (66 ± 4.8 years) and 14 healthy controls (65 ± 5.5 years) underwent T1 and T2 magnetic resonance imaging, along with (11)C-(R)-PK11195, (11)C-Pittsburgh compound B and (18)F-fluorodeoxyglucose positron emission tomography scans for microglial activation, amyloid deposition and glucose metabolism. All patients were followed-up with repeated magnetic resonance imaging and three positron emission tomography scans after 16 months. Parametric maps were interrogated using region of interest analysis, Statistical Parametric Mapping, and between-group correlation analysis at voxel-level using Biological Parametric Mapping. At baseline, patients with Alzheimer's disease showed significantly increased microglial activation compared to the control subjects. During follow-up, for the first time, we found that while there is a progressive reduction of glucose metabolism, there was a longitudinal increase of microglial activation in the majority of the patients with Alzheimer's disease. Voxel-wise correlation analysis revealed that microglial activation in patients with Alzheimer's disease was positively correlated with amyloid deposition and inversely correlated with regional cerebral metabolic rate at voxel level over time. Even though one of the limitations of this study is the lack of longitudinal follow-up of healthy control subjects, this study demonstrates that there is persistent neuroinflammation throughout the Alzheimer's disease process with associated synaptic dysfunction and reduced glucose metabolism. Voxel-wise correlation analysis suggests that neuroinflammation is associated with localized amyloid deposition and glucose metabolism over time, however, the level of inflammation could also occur independently of amyloid pathology, especially in the later stages of Alzheimer's disease.
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In Alzheimer's disease patients, microglial activation correlates with glucose hypometabolism, suggesting a link between microglial activation and synaptic dysfunction.
“microglial activation correlated with glucose hypometabolism in AD patients (103), suggesting a link between microglial activation and synaptic dysfunction.”
From Microglia in Alzheimer's disease (2017) · cites this paper as [103]
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- Authors
- Fan, Z., Okello, A. A., Brooks, D. J., & Edison, P.
- Affiliations
- Hammersmith Hospital (GB)
- Aarhus University (DK)
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-10-27
- Volume
- 138
- Issue
- 12
- Pages
- 3685-3698
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W1820933137
- Cited by
- 135
- References
- 51
- Citations by year
- 2026: 5 · 2025: 17 · 2024: 7 · 2023: 12 · 2022: 11 · 2021: 12 · 2020: 15 · 2019: 16 · 2018: 16 · 2017: 15 · 2016: 9
- FWCI
- 7.11
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- Funders
- National Institute for Health and Care Research
- 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
- Alzheimer's disease, microglial activation, amyloid deposition, neuroinflammation, glucose metabolism, longitudinal disease progression, synaptic dysfunction, Pittsburgh compound B, PK11195, FDG-PET
- MeSH terms
- Aged, Alzheimer Disease, Amyloid, Aniline Compounds, Brain, Female, Follow-Up Studies, Glucose, Humans, Isoquinolines, Male, Middle Aged, Neurons, Thiazoles, Case-Control Studies, Microglia, Disease Progression, Fluorodeoxyglucose F18, Positron-Emission Tomography, Functional Neuroimaging
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