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Fig. 5 | Acta Neuropathologica Communications

Fig. 5

From: Aggregate-selective antibody attenuates seeded aggregation but not spontaneously evolving disease in SOD1 ALS model mice

Fig. 5

αSOD1143–153 does not attenuate spontaneous aggregation and ALS-like disease in hSOD1G85R Tg mice. a Outline of the mAb injection scheme in the hSOD1G85R Tg mouse model (non-seed inoculated mice): once weekly peripheral administration of mAbs via i.p injections was initiated before accumulation of detectable SOD1 aggregation (d250) and continued until mice reached the paralytic end-stage. b Kaplan–Meier plot showing survival in days. There was no significant difference between curves (n = 9–10 animals/group). Survival of non-treated hSOD1G85R Tg mice included for comparison (black dotted line). See also supplementary table S3. Graphs represent: c level of soluble hSOD1 in cervical spinal cord samples determined by western blot. Values were normalized to total protein in the samples determined by BCA assay. mAb treatment did not result in significantly lowered levels of soluble hSOD1 (n = 6 animals/group). d Level of aggregated hSOD1 in cervical spinal cord analyzed by dot blot using rbAb SOD157–72. mAb treatment had no significant effect on aggregate load in terminal stage in hSOD1G85R Tg mice (n = 6 animals/group). e Conformation of hSOD1 aggregates in spinal cord samples determined by binary epitope mapping. Bars represent the mean reactivity of the 8 peptide antibodies used to probe filter trapped spinal cord derived aggregates from the respective treatment group: Vehicle treatment (black): 50 mg/kg αSOD1143–153 (red); 50 mg/kg IgG1 (grey) (n = 6 animals/group). Relative binding to the hSOD1 sequences is presented as the percentage of rbAb SOD157–72 binding (set as 100%). mAb treatment did not alter the conformation of strain A aggregates forming in the hSOD1G85R Tg spinal cord

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