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Lysosomal storage diseases (LSDs) encompass a wide range of disorders characterized by inborn errors of lysosomal function. The majority of LSDs result from genetic defects in lysosomal enzymes, although some arise from mutations in lysosomal proteins that lack known enzymatic activity. Neuropathological abnormalities are a feature of several LSDs and when severe, represent an important determinant in disease outcome. Glial dysfunction, particularly in astrocytes, is also observed in numerous LSDs and has been suggested to impact neurodegeneration. This review will discuss the potential role of astrocytes in LSDs and highlight the possibility of targeting glia as a beneficial strategy to counteract the neuropathology associated with LSDs. [ABSTRACT FROM AUTHOR]

The article presents abstracts of research papers about the effects of neuroinflammation on gap junction communication. They include "Connexins and neuroprotection: minding the gap," "Connexins regulate gene expression: how, why, and implications for neuroinflammation," "Astrocyte gap junctions are a target for pro-inflammatory cytokines released from microglial cells," and "The gram-positive bacterium S. aureus differentially modulates gap junction communication in astrocytes and microglia."