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. Author manuscript; available in PMC: 2020 Jul 15.
Published in final edited form as: Neuroscience. 2019 May 23;411:1–10. doi: 10.1016/j.neuroscience.2019.05.029

Figure 3. FTY720 reduces synucleinopathy, increases BDNF protein, and sustains MBP and CNP at younger levels in aging GM2+/− brachial plexus.

Figure 3.

(A) aSyn immunoblot from representative vehicle (Veh) treated GM2+/− mice shows abundant high molecular weight (HMW) aSyn, which is eliminated in brachial plexus of age matched FTY720 treated GM2+/− mice. (B) Quantification of total aSyn and pathological PSer129 aSyn from multiple brachial plexus samples confirms a significant reduction in synucleinopathy in FTY720 treated GM2+/− mice compared to vehicle treated GM2+/− mice. (C) Reprobing the immunoblot shown in A for BDNF, confirms FTY720 increased preproBDNF and proBDNF levels in brachial plexus, as compared to vehicle treated GM2+/− mice. (D) Myelin associated proteins MBP and CNP are abundant in brachial plexus of untreated 9 mo mouse, absent in 17 mo vehicle treated GM2+/mouse, and sustained in 17 mo GM2+/− mouse treated with FTY720. Student’s t test, **, p < 0.01; ***, p < .001.