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Innate immunity in amyotrophic lateral sclerosis
Although the underlying cause remains unclear, evidence suggests a role for innate immunity in disease pathogenesis. Neuroinflammation in areas of motor neuron loss is evident in presymptomatic mouse models of ALS and in human patients.

Modulating inflammatory monocytes with a unique microRNA gene signature ameliorates murine ALS.
Prior to disease onset, splenic Ly6Chi monocytes expressed a polarized macrophage phenotype (M1 signature), which included increased levels of chemokine receptor CCR2.

Progressive changes in microglia and macrophages in spinal cord and peripheral nerve in the transgenic rat model of amyotrophic lateral sclerosis.
Our study reveals an accumulation of microglia/macrophages both in the spinal cord and peripheral nerve prior to clinical onset based on CD11b tissue expression.

Appearance of phagocytic microglia adjacent to motoneurons in spinal cord tissue from a presymptomatic transgenic rat model of amyotrophic lateral sclerosis.
In this study, we revealed that activated microglia aggregated in the lumbar spinal cord of presymptomatic mutant SOD1(H46R) transgenic rats, an animal model of familial ALS.

The Neuroinflammatory Response in ALS: The Roles of Microglia and T Cells.
In the mSOD mouse, increased numbers of activated microglia are observed at early presymptomatic stages of disease, and with disease progression to end-stage, microglial numbers in the lumbar spinal cord increase further by nearly 2-fold.