Lysosomal and phagocytic activity is increased in astrocytes during disease progression in the SOD1 (G93A) mouse model of amyotrophic lateral sclerosis.

The complement pathway consists of a cascade of protein activation, centered around C1q, the three components of which (C1qa, b, and c) are up-regulated at symptomatic and further at late-stages in our microarray of astrocytes with C1q and C4b showing the most highly significant differential expression ( p ≤ 0.0001) of all dysregulated genes at late stage disease.

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