Association of cholinergic basal forebrain volume and functional connectivity with markers of inflammatory response in the Alzheimer’s disease spectrum
Open accessAbstract
BACKGROUND: Inflammation has been described as a key pathogenic event in Alzheimer's disease (AD), downstream of amyloid and tau pathology. Preclinical and clinical data suggest that the cholinergic basal forebrain may moderate inflammatory response to different pathologies. OBJECTIVE: To study the association of cholinergic basal forebrain volume and functional connectivity with measures of neuroinflammation in people from the AD spectrum. METHODS: We studied 261 cases from the DELCODE cohort, including people with subjective cognitive decline, mild cognitive impairment, AD dementia, first degree relatives, and healthy controls. Using Bayesian ANCOVA, we tested associations of MRI indices of cholinergic basal forebrain volume and functional connectivity with cerebrospinal fluid (CSF) levels of sTREM2 as a marker of microglia activation, and serum levels of complement C3. Using Bayesian elastic net regression, we determined associations between basal forebrain measures and a large inflammation marker panel from CSF and serum. RESULTS: We found anecdotal to moderate evidence in favor of the absence of an effect of basal forebrain volume and functional connectivity on CSF sTREM2 and serum C3 levels both in Aβ42/ptau-positive and negative cases. Bayesian elastic net regression identified several CSF and serum markers of inflammation that were associated with basal forebrain volume and functional connectivity. The effect sizes were moderate to small. CONCLUSION: Our data-driven analyses generate the hypothesis that cholinergic basal forebrain may be involved in the neuroinflammation response to Aβ42 and phospho-tau pathology in people from the AD spectrum. This hypothesis needs to be tested in independent samples.
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A majority of Alzheimer's disease risk genes identified through genome-wide association studies are highly expressed in microglia, suggesting a key role in microglial dysfunction.
“A majority of AD risk genes identified through genome-wide association studies are highly expressed in microglia, the brain’s innate immune cells, suggesting a key role in microglial dysfunction (Kummer et al., 2021; Penney et al., 2020; Teipel et al., 2022).”
From A novel molecular class that recruits HDAC/MECP2 complexes to PU.1 motifs reduces neuroinflammation (2023) · cites this paper as Teipel et al., 2022
The Introduction discusses microglia-derived inflammatory factors in Alzheimer’s disease, and the Discussion addresses markers of microglial activation, but neither addresses expression of AD risk genes in microglia. Searches for genome-wide association studies and microglial expression of genetic risk genes found no passage supporting the claimed majority. (LLM, conf=0.75)
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A novel molecular class that recruits HDAC/MECP2 complexes to PU.1 motifs reduces neuroinflammation
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- Authors
- Teipel, S. J., Dyrba, M., Ballarini, T., Brosseron, F., Bruno, D., Buerger, K., Cosma, N.-C., Dechent, P., Dobisch, L., Düzel, E., Ewers, M., Fliessbach, K., Haynes, J. D., Janowitz, D., Kilimann, I., Laske, C., Maier, F., Metzger, C. D., Munk, M. H., Peters, O., Pomara, N., Preis, L., Priller, J., Ramírez, A., Roy, N., Scheffler, K., Schneider, A., Schott, B. H., Spottke, A., Spruth, E. J., Wagner, M., Wiltfang, J., Jessen, F., & Heneka, M. T.
- Affiliations
- German Center for Neurodegenerative Diseases (DE)
- University Hospital Bonn (DE)
- Liverpool John Moores University (GB)
- German Center for Neurodegenerative Diseases (DZNE), Munich, Germany
- Stiftung Charité (DE)
- University of Göttingen (DE)
- Bernstein Center for Computational Neuroscience Berlin (DE)
- Institut für Schlaganfall- und Demenzforschung (DE)
- University of Cologne (DE)
- Nathan Kline Institute for Psychiatric Research (US)
- German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany
- University of Tübingen (DE)
- ORCID
- Teipel, Stefan J.
- Dyrba, Martin
- Ballarini, Tommaso
- Brosseron, Frederic
- Bruno, Davide
- Cosma, Nicoleta-Carmen
- Dechent, Peter
- Düzel, Emrah
- Fliessbach, Klaus
- Haynes, John D.
- Janowitz, Daniel
- Kilimann, Ingo
- Laske, Christoph
- Maier, Franziska
- Munk, Matthias H.
- Peters, Oliver
- Pomara, Nunzio
- Preis, Lukas
- Priller, Josef
- Scheffler, Klaus
- Schneider, Anja
- Schott, Björn H.
- Spottke, Annika
- Spruth, Eike J.
- Wagner, Michael
- Wiltfang, Jens
- Jessen, Frank
- Heneka, Michael T.
- Venue
- Journal of Alzheimer s Disease
- Publisher
- SAGE Publications
- Published
- 2022-02-01
- Volume
- 85
- Issue
- 3
- Pages
- 1267-1282
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W4200291023
- Cited by
- 20
- References
- 64
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 5 · 2022: 8
- FWCI
- 1.70
- Type
- journal article
- Language
- en
- Open access
- Licence
- other-oa
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- Liverpool John Moores University (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion)
- DZNE Pub (submittedVersion)
- GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion, other-oa)
- 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
- basal forebrain cholinergic system, neuroinflammation
- MeSH terms
- Aged, Alzheimer Disease, Female, Humans, Inflammation, Magnetic Resonance Imaging, Male, Cohort Studies, Biomarkers, Cholinergic Agents, Cognitive Dysfunction, Basal Forebrain
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