2011
DOI: 10.4161/auto.7.4.14541
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Rapamycin treatment augments motor neuron degeneration in SOD1G93Amouse model of amyotrophic lateral sclerosis

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Cited by 330 publications
(292 citation statements)
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“…Our previous studies showed that the mTOR-dependent autophagic inducer rapamycin accelerates motor neuron loss and aggravates autophagic flux dysfunction in the SOD1 G93A mouse model of ALS [11] . Our latest report provided strong evidence for an autophagic flux defect, especially impairment in the fusion of autophagosomes and lysosomes in the ALS model [12] .…”
Section: Discussionmentioning
confidence: 99%
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“…Our previous studies showed that the mTOR-dependent autophagic inducer rapamycin accelerates motor neuron loss and aggravates autophagic flux dysfunction in the SOD1 G93A mouse model of ALS [11] . Our latest report provided strong evidence for an autophagic flux defect, especially impairment in the fusion of autophagosomes and lysosomes in the ALS model [12] .…”
Section: Discussionmentioning
confidence: 99%
“…Transgenic SOD1 G93A mice expressing mutant human SOD1 with a Gly93Ala substitution (B6SJL-Tg-SOD1G93A-1Gur) were originally obtained from Jackson Laboratories The genotypes of the transgenic mice were identifi ed by PCR as in our previous reports [11,12] . Male SOD1 G93A mice were randomly divided into 2 groups (Tg-Control and Tg-HDAC6, 18 mice in each).…”
Section: Mice and Treatmentsmentioning
confidence: 99%
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