The Amyloid Inhibitor CLR01 Relieves Autophagy and Ameliorates Neuropathology in a Severe Lysosomal Storage Disease

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(Molecular Therapy 28, 1167–1176; April 2020) In the originally published version of this article, an error was made during the assembly of Figure 4A: the cropped image used as representative of "striatum anti-GFAP WT + saline" was inadvertently taken from the folder containing the cropped images of "striatum anti-GFAP WT + CLR01" fields, instead of from the correct folder (cropped images of “striatum anti-GFAP WT + saline” fields). Therefore, two partial overlapping cropped images of the same field (striatum anti-GFAP WT + CLR01) were used in the panel. The correct version of Figure 4A is included here. The authors apologize for the error. The Amyloid Inhibitor CLR01 Relieves Autophagy and Ameliorates Neuropathology in a Severe Lysosomal Storage DiseaseMonaco et al.Molecular TherapyFebruary 11, 2020In BriefFraldi and colleagues demonstrated that multiple amyloid proteins progressively aggregate in neurons of a severe lysosomal storage disease, impairing autophagy degradation and triggering neurodegeneration. They also showed that inhibiting amyloid deposition protects against neurodegeneration, thus providing evidence that amyloid aggregation is a new attractive target for the treatment of LSDs. Full-Text PDF Open Access

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