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. 2014 May 27;124(7):3032–3046. doi: 10.1172/JCI72176

Figure 6. Genetic inhibition of Aldh1a1 promotes α-synuclein aggregation in A53T transgenic mice.

Figure 6

(A) Human α-synuclein and ALDH1A1 costaining in the nontreated or PK-treated DL striatum sections of 18-month-old A53T/Aldh1a1+/+ and A53T/Aldh1a1–/– mice. Scale bar: 10 μm. (B and C) The average intensity of α-synuclein signals in the axon fibers of (B) nontreated and (C) PK-treated DL striatum sections of 18-month-old A53T/Aldh1a1+/+ and A53T/Aldh1a1–/– female mice (n = 3 animals per genotype). (D) Western blot shows the formation of α-synuclein–positive HMW bands in the striatum homogenate of 6-month-old A53T/Aldh1a1+/+ and A53T/Aldh1a1–/– mice. (E) The relative intensity of HMW α-synuclein bands (n = 3 female mice per genotype). (F) A Western blot of α-synuclein from the APBA pull-down experiment shows the enrichment of DOPAL-modified α-synuclein in 6-month-old A53T/Aldh1a1+/+ and A53T/Aldh1a1–/– mice. (G) The graph indicates an increase of accumulation of HMW DOPAL-modified α-synuclein in brains of A53T/Aldh1a1–/– mice compared with littermate A53T/Aldh1a1+/+ mice (n = 3 pairs females). *P < 0.05, ***P < 0.001.