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Plasma MCP-1 and changes on cognitive function in community-dwelling older adults
Juan Luis Sanchez-Sanchez1,2, Kelly V Giudici1, Sophie Guyonnet1,3
1Gérontopôle de Toulouse, Institut du Vieillissement, Centre Hospitalier-Universitaire de Toulouse, 37 allées Jules Guesde, 31000, Toulouse, France.
Plasma Monocyte Chemoattractant Protein-1 (MCP-1) is linked to cognitive decline in older adults. Higher MCP-1 levels correlate with worsening memory, especially when amyloid plaques are present.
Area of Science:
- Neuroscience
- Immunology
- Gerontology
Background:
- Monocyte Chemoattractant Protein-1 (MCP-1) is a glial-derived chemokine implicated in neuroinflammation.
- MCP-1 may influence memory function in aging populations.
- Understanding MCP-1's role in cognitive decline is crucial for developing targeted interventions.
Purpose of the Study:
- To investigate the association between plasma MCP-1 levels and cognitive changes in older adults.
- To explore the combined effect of MCP-1 and beta-amyloid (Aβ42/40) on cognitive trajectories.
- To determine if MCP-1 predicts declines in overall and domain-specific cognitive functions.
Main Methods:
- Analysis of 1097 participants from the Multidomain Alzheimer Preventive Trial (MAPT).
- Measurement of plasma MCP-1 and Aβ42/40 levels at baseline.
- Assessment of cognitive function annually over 4 years using composite scores, MMSE, CDR, and FCSRT.
Main Results:
- Elevated plasma MCP-1 levels were associated with worsening episodic memory, particularly delayed recall.
- Higher MCP-1 levels correlated with declines in overall cognitive function (CCS and CDR).
- The association between MCP-1 and cognitive decline was more pronounced in individuals with lower Aβ42/40 levels, suggesting an interaction.
Conclusions:
- Baseline plasma MCP-1 levels predict longitudinal declines in cognitive and episodic memory performance in older adults.
- The interaction between MCP-1 and Aβ42/40 warrants further investigation to understand their combined impact on cognitive decline.
- MCP-1's impact on cognitive decline is amplified in the presence of amyloid pathology, as indicated by plasma Aβ42/40.
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