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GM-CSF Upregulated in Rheumatoid Arthritis Reverses Cognitive Impairment and Amyloidosis in Alzheimer Mice
Open accessAbstract
Rheumatoid arthritis (RA) is a negative risk factor for the development of Alzheimer's disease (AD). While it has been commonly assumed that RA patients' usage of non-steroidal anti-inflammatory drugs (NSAIDs) helped prevent onset and progression of AD, NSAID clinical trials have proven unsuccessful in AD patients. To determine whether intrinsic factors within RA pathogenesis itself may underlie RA's protective effect, we investigated the activity of colony-stimulating factors, upregulated in RA, on the pathology and behavior of transgenic AD mice. 5 microg bolus injections of macrophage, granulocyte, and granulocyte-macrophage colony-stimulating factors (M-CSF, G-CSF, or GM-CSF) were administered unilaterally into the hippocampus of aged cognitively-impaired AD mice and the resulting amyloid load reductions determined one week later, using the artificial cerebrospinal fluid-injected contralateral sides as controls. G-CSF and more significantly, GM-CSF reduced amyloidosis throughout the treated brain hemisphere one week following bolus administration to AD mice. 20 daily subcutaneous injections of 5 microg of GM-CSF (the most amyloid-reducing CSF in the bolus experiment) were administered to balanced cohorts of AD mice after assessment in a battery of cognitive tests. Reductions in amyloid load and improvements in cognitive function were assessed. Subcutaneous GM-CSF administration significantly reduced brain amyloidosis and completely reversed the cognitive impairment, while increasing hippocampal synaptic area and microglial density. These findings, along with two decades of accrued safety data using Leukine, recombinant human GMCSF, in elderly leukopenic patients, suggest that Leukine should be tested as a treatment to reverse cerebral amyloid pathology and cognitive impairment in AD.
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“In contrast, the levels of antiageing factors, such as GDF11, tissue inhibitor of metalloproteinase 2 (TIMP2) and granulocyte‒macrophage colony stimulating factor (CSF2), are reduced. These factors are linked to improved microglial phagocytosis and neurogenesis and reduce the Aβ load, thus enhancing cognition.72,322–324”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [323]
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Metadata
- Authors
- Boyd, T. D., Bennett, S. P., Mori, T., Governatori, N., Runfeldt, M., Norden, M., Padmanabhan, J., Neame, P., Wefes, I., Sanchez-Ramos, J., Arendash, G. W., & Potter, H.
- Affiliations
- University of South Florida (US)
- Social Insurance Saitama Chuo Hospital (JP)
- USF Health Byrd Alzheimer's Center and Research Institute, Tampa, FL, USA
- Corresponding author
- Potter, Huntington
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2010-08-11
- Volume
- 21
- Issue
- 2
- Pages
- 507-518
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC5588158
- OpenAlex
- W2142301391
- Cited by
- 128
- References
- 46
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 12 · 2023: 4 · 2022: 10 · 2021: 9 · 2020: 6 · 2019: 10 · 2018: 8 · 2017: 8 · 2016: 11 · 2015: 6 · 2014: 5 · 2013: 6 · 2012: 14
- FWCI
- 5.20
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Commons - University of South Florida (University of South Florida) (submittedVersion)
- Funders
- Japan Society for the Promotion of Science (22500320)
- National Institute on Aging (P50 AG25711, P50AG025711)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- rheumatoid arthritis, Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Amyloidosis, Animals, Arthritis, Rheumatoid, Cognition Disorders, Disease Models, Animal, Hippocampus, Humans, Mice, Inbred C57BL, Mice, Transgenic, Risk Factors, Up-Regulation, Macrophage Colony-Stimulating Factor, Granulocyte-Macrophage Colony-Stimulating Factor, Granulocyte Colony-Stimulating Factor, Maze Learning, Mice
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