From: buerstatteamada@gmail.com   
      
   Microfluidic chambers facilitate the isolation of axonal terminals from cell   
   bodies in culture modelling pathology along the neuron from synapse to soma.   
   Several studies have shown that degeneration may start in the striatal axons   
   before affecting the    
   cell soma of dopaminergic neurons33. In support of this theory, neuroimaging   
   studies have shown that human PD presents early with a larger loss of   
   transporters and other DA axon markers in the striatum than in the SNc34,35.   
   As a result several groups    
   have studied this early degeneration in α-syn overexpression mouse models and   
   shown early striatal synaptic and dopamine release defects prior to   
   neurodegeneration12,36. It is therefore important to investigate in vitro and   
   in vivo whether the toxic    
   effects of α-syn on axon terminals can be alleviated with CLR01   
   administration. Using microfluidic chambers in vitro, we observed that CLR01   
   reduced the accumulation of α-syn oligomers in the cell soma after treatment   
   of axonal terminals, although it    
   is possible that this was in part due to an inhibition of retrograde transport   
   of α-syn, or to the minimal flow of CLR01-containing medium to the insult   
   chamber. In parallel studies in vivo, CLR01 administration reduced lesions in   
   dopaminergic cell    
   somas in the SNc after injection of mPFFs to the dorsal striatum, confirming a   
   protective effect of CLR01 against α-syn pathology in both axons and cell   
   bodies.   
      
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