Plasma IL-12/IFN-γ axis predicts cognitive trajectories in cognitively unimpaired older adults
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Introduction: Immune dysregulation is implicated in neurodegeneration and altered cytokine levels are seen in people with dementia. However, whether cytokine levels are predictive of cognitive decline in cognitively unimpaired (CU) elderly, especially in the setting of elevated amyloid beta (Aβ), remains unclear. Methods: We measured nine cytokines in the baseline plasma of 298 longitudinally followed CU elderly and assessed whether these measures were associated with cognitive decline, alone or synergistically with Aβ. We next examined associations between cytokine levels and neuroimaging biomarkers of Aβ/tau/neurodegeneration. Results: Higher IL‐12p70 was associated with slower cognitive decline in the setting of higher Aβ (false discovery rate [FDR] = 0.0023), whereas higher IFN‐γ was associated with slower cognitive decline independent of Aβ (FDR = 0.013). Higher IL‐12p70 was associated with less tau and neurodegeneration in participants with higher Aβ. Discussion: Immune dysregulation is implicated in early‐stage cognitive decline, and greater IL‐12/IFN‐γ axis activation may be protective against cognitive decline and early‐stage AD progression.
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Higher levels of IFN-γ and IL-12 (Th1 cytokines) were recently associated with slower cognitive decline in older adults.
“Counterintuitively, higher levels of IFN-γ and IL-12 (Th1 cytokines) were recently associated with slower cognitive decline in older adults, suggesting that the contribution of inflammatory signaling to neurodegenerative disease is complex and likely dependent on the inflammatory mediator in question (153).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [153]
Studies have demonstrated that a proinflammatory state, inflammatory disease (e.g., rheumatoid arthritis), and immune challenges (e.g., acute infection) all increase the risk for dementia over multiple decades.
“Studies have demonstrated that a proinflammatory state (148–150), inflammatory disease (e.g., rheumatoid arthritis) (151), and immune challenges (e.g., acute infection) (152, 153) all increase the risk for dementia over multiple decades.”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [153]
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- Authors
- Yang, H., Zhang, C., Carlyle, B. C., Zhen, S. Y., Trombetta, B. A., Schultz, A. P., Pruzin, J. J., Fitzpatrick, C. D., Yau, W. W., Kirn, D. R., Rentz, D. M., Arnold, S. E., Johnson, K. A., Sperling, R. A., Chhatwal, J. P., & Tanzi, R. E.
- Affiliations
- Brigham and Women's Hospital (US)
- Harvard University (US)
- Massachusetts General Hospital (US)
- Corresponding author
- Chhatwal, Jasmeer P.
- Tanzi, Rudolph E.
- ORCID
- Venue
- Alzheimer's & Dementia
- Publisher
- Wiley
- Published
- 2021-06-23
- Volume
- 18
- Issue
- 4
- Pages
- 645-653
- ISSN
- 1552-5260 (ISSN-L)
- 1552-5279
- PMC
- PMC8695625
- OpenAlex
- W3113147893
- Cited by
- 90
- References
- 41
- Citations by year
- 2026: 9 · 2025: 19 · 2024: 28 · 2023: 18 · 2022: 12 · 2021: 4
- FWCI
- 11.11
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Alzheimer s & Dementia (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (P01 AG036694, K23 AG049087, K23 AG062750, K24 AG035007, R01 AG062667)
- Cure Alzheimer's Fund
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- IL-12p70
- MeSH terms
- Aged, Alzheimer Disease, Cognition, Humans, Biomarkers, Amyloid beta-Peptides, tau Proteins, Interleukin-12, Positron-Emission Tomography, Cognitive Dysfunction
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