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

Figure 2. ALDH1A1-negative nigrostriatal DA neurons contain more PK-resistant α-synuclein aggregates in soma and axon fibers.

Figure 2

(A) Western blot shows α-synuclein aggregation induced by application of DOPAL (1 mM) for various time periods as well as the level of monomeric α-synuclein with shorter exposure. HMW, high molecular weight. (B) Human α-synuclein (hα-syn) (green) and ALDH1A1 (red) costaining in the nontreated or PK-treated SNpc coronal sections of 12-month-old female A53T mice. Topro3 staining (blue) was used to mark the nucleus. The asterisks indicate an ALDH1A1-negative nigrostriatal DA neuron with substantial deposition of α-synuclein aggregates. Arrows mark the ALDH1A1-positive nigrostriatal DA neurons with less accumulation of α-synuclein aggregates. (C and D) The average intensity of α-synuclein signals in the soma of (C) nontreated and (D) PK-treated ALDH1A1-positive (+) and negative (–) nigrostriatal DA neurons of 12-month-old A53T female mice (n ≥ 3 animals per genotype and ≥40 neurons per animal). ***P < 0.001. (E) Dot plot correlates the level of α-synuclein (y axis) and ALDH1A1 (x axis) expression in 115 nontreated and 89 PK-treated neurons in SNpc sections of 12-month-old A53T female mice. (F) Human α-synuclein (green) and ALDH1A1 (red) costaining in the nontreated or PK-treated DL striatum sections of 12-month-old A53T female mice. The numbers mark the cross points of white lines with nigrostriatal DA axon fibers that correlate with the peaks of histograms of α-synuclein (green) and ALDH1A1 (red) signals at individual fibers. Scale bar: 10 μm (B and F).