Amyotrophic lateral sclerosis (ALS) is a progressive disease wherein the cells of the central nervous system (CNS) involved in movement and coordination are destroyed. Although the mechanism of ALS is not completely understood, inflammation is believed to play a role in the disease process.
A recent study by Howard Weiner and colleagues at Harvard Medical School and Tufts School of Medicine investigated the role of inflammation in a mouse model of ALS. Weiner and colleagues found that the recruitment of activated immune cells known as monocytes into the spinal cord correlated with increased CNS cell death, and this recruitment was mediated by high expression of the chemoattractant protein CCL2 by resident spinal cord-derived immune cells.
Antibody-mediated depletion of the monocyte population reduced cellular recruitment to the spinal cord, decreased CNS cell death, and extended survival time in the mice. The analogous monocyte population in humans with ALS exhibited a similar inflammatory signature to the ALS model mice, suggesting that this cell population could serve as a marker of disease progression in human ALS patients. Thus, these results identify an inflammatory monocyte population as a potential therapeutic target for ALS.
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