Cromolyn Reduces Levels of the Alzheimer’s Disease-Associated Amyloid β-Protein by Promoting Microglial Phagocytosis
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Amyloid-beta protein (Aβ) deposition is a pathological hallmark of Alzheimer’s disease (AD). Aβ deposition triggers both pro-neuroinflammatory microglial activation and neurofibrillary tangle formation. Cromolyn sodium is an asthma therapeutic agent previously shown to reduce Aβ levels in transgenic AD mouse brains after one-week of treatment. Here, we further explored these effects as well as the mechanism of action of cromolyn, alone, and in combination with ibuprofen in APP Swedish-expressing Tg2576 mice. Mice were treated for 3 months starting at 5 months of age, when the earliest stages of β-amyloid deposition begin. Cromolyn, alone, or in combination with ibuprofen, almost completely abolished longer insoluble Aβ species, i.e. Aβ40 and Aβ42, but increased insoluble Aβ38 levels. In addition to its anti-aggregation effects on Aβ, cromolyn, alone, or plus ibuprofen, but not ibuprofen alone, increased microglial recruitment to, and phagocytosis of β-amyloid deposits in AD mice. Cromolyn also promoted Aβ42 uptake in microglial cell-based assays. Collectively, our data reveal robust effects of cromolyn, alone, or in combination with ibuprofen, in reducing aggregation-prone Aβ levels and inducing a neuroprotective microglial activation state favoring Aβ phagocytosis versus a pro-neuroinflammatory state. These findings support the use of cromolyn, alone, or with ibuprofen, as a potential AD therapeutic.
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In an in vivo AD mouse model, the cromolyn-ibuprofen combination showed better effects than cromolyn or ibuprofen alone.
“An efficacy study in in vivo AD mouse model evidenced better effects of the drug combination compared with cromolyn and ibuprofen alone.59”
From From combinations to multitarget-directed ligands: A continuum in Alzheimer’s disease polypharmacology (2021) · cites this paper as [59]
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Self-citation
- Authors
- Zhang, C., Griciuc, A., Hudry, E., Wan, Y., Quinti, L., Ward, J., Forte, A. M., Shen, X., Ran, C., Elmaleh, D. R., & Tanzi, R. E.
- Affiliations
- Harvard University (US)
- Corresponding author
- Tanzi, Rudolph E.
- Venue
- Scientific Reports
- Published
- 2018-01-18
- Volume
- 8
- Issue
- 1
- Pages
- 1144-1144
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5773545
- OpenAlex
- W2782619707
- Cited by
- 99
- References
- 32
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 9 · 2023: 15 · 2022: 15 · 2021: 16 · 2020: 14 · 2019: 6 · 2018: 3 · 2017: 1
- FWCI
- 6.69
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Cure Alzheimer's Fund
- National Institute on Aging (R00AG047336)
- Topics
- Health Sciences › Medicine › Physiology › 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
- disodium cromoglycate, amyloid-beta, Alzheimer's disease, microglial phagocytosis, ibuprofen, amyloid-beta aggregation, amyloid-beta 42, Aβ40, microglial recruitment, neuroinflammation, Tg2576 mice, anti-aggregation therapy
- MeSH terms
- Alzheimer Disease, Animals, Brain, Disease Models, Animal, Cromolyn Sodium, Drug Combinations, Humans, Ibuprofen, Male, Mice, Transgenic, Neurons, Peptide Fragments, Phagocytosis, Gene Expression, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Microglia, Neuroprotective Agents, Anti-Asthmatic Agents, Transgenes, Mice, Drug Repositioning
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