Wegrzynowicz M, et al. - In order to enhance understanding of the relationship between progressive α-synuclein (αSyn) aggregation and mechanisms of Parkinson’s disease (PD), researchers sought to create and describe a novel transgenic mouse model of PD and allow testing of prospective therapies for α-synucleinopathies. Under the control of the tyrosine hydroxylase promoter, a new transgenic mouse line (MI2) expressing human, aggregation-prone truncated 1–120 αSyn was made. For studying structural/morphological changes connected to aggregate toxicity, MI2 mice were considered an appropriate model and a useful method. Even when striatal dopamine release is already impaired, there time period when dopamine neuronal death can be prevented, as indicated through this study. The model recapitulates the progressive αSyn aggregation and DA neuron dysfunction and death observed in human PD. By disrupting αSyn aggregate formation, anle138b restored DA function, rescued several gait abnormalities and prevented nerve cell loss.