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Increased chemokine gene expression during aging in the murine brain
L K Felzien1, J T McDonald, S M Gleason
1Department of Anatomy and Cell Biology, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA. lisa.felzien@rockhurst.edu
Brain Research
|February 13, 2001
Summary
Brain aging leads to cognitive decline. This study found increased chemokine expression and microglial activation in aging mouse brains, suggesting a link to memory loss.
Area of Science:
- Neuroscience
- Immunology
- Aging Research
Background:
- Normal brain aging is associated with functional decline, particularly in learning and memory.
- The underlying mechanisms of age-related cognitive decline remain unclear.
- Microglial activation, a component of the aging process, can produce detrimental substances.
Purpose of the Study:
- To investigate changes in chemokine gene expression during normal aging in the mouse brain.
- To determine if specific chemokines are upregulated in aging brains.
- To correlate chemokine expression with microglial activation.
Main Methods:
- Gene expression analysis (RNase protection assays) of mouse brain regions (cortex, midbrain, hippocampus, cerebellum) at different ages (4, 10, 21, 30 months).
- Protein level quantification using ELISA.
- Immunohistochemistry with F4/80 antibodies to assess microglial activation.
Main Results:
- Significant increases in macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and RANTES gene expression were observed in all brain regions of the oldest mice (30 months).
- These chemokine increases were detectable starting at 21 months of age.
- Elevated protein levels of these chemokines and increased microglial activation were confirmed in aged brains.
Conclusions:
- Chemokine gene expression, specifically MIP-1alpha, MIP-1beta, and RANTES, is upregulated during normal mouse brain aging.
- Increased microglial activation correlates with elevated chemokine levels in aging brains.
- These findings suggest that chemokines may play a role in age-related cognitive decline.