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Description
PMID 31672538
For instance, the M83 mouse expressing mutant human syn demonstrates that abnormal syn accumulation is sufficient to drive neurodegenerative phenotypes including neuronal hyperactivity and vascular patterning defects, even in the absence of overt systemic inflammation [164, 165]
& Horne, A
Our findings show that the depletion of GSH by TNBS is a necessary but insufficient event by itself to cause injury
Possession and use for personal research is generally legal, but regulations vary by location
this necessitates a distinct focus in our analysis
