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In this issue

Multiple system atrophy (MSA) is a sporadic neurodegenerative disease that may manifest with parkinsonism (MSA-P), cerebellar ataxia (MSA-C) or autonomic dysfunction. Pathologically, the disease is characterised by a-synuclein positive glial cytoplasmic inclusions (GCI) within oligodendrocytes and with variable anatomical patterns of involvement, in particular striatonigral and olivopontocerebellar degeneration. In their comprehensive paper, Ahmed et al. review the neuropathology, pathophysiology and genetics of this relentless disease. They consider in vivo and in vitro modelling approaches and discuss the roles of a-synuclein, toxic stressors, microglial-derived neuroinflammation and p25a, an important molecule in myelination and oligodendrocyte biology. They also discuss the literature and current studies into genetic influences on this disease.