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In a transgenic mouse model of mutant alpha-synuclein (A53T), experiments showed that alpha-synuclein accumulation in astrocytes affected glutamate transport, triggering a rise of extracellular glutamatergic concentrations and excitotoxicity, which further exacerbated damage to dopaminergic neurons (Gu et al., 2010)

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Altogether, zebrafish models can well resemble the growth and the aggressiveness of MB in humans to analyze the effects on MB biology due to the genome editing and the presence of specific mutation and/or activation of oncogenes (130134) ( Figure 1 )