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Brain Pathol. 2017 Jan;27(1):86-94. doi: 10.1111/bpa.12368. Epub 2016 Jun 13.

Targeted Antioxidant, Catalase-SKL, Reduces Beta-Amyloid Toxicity in the Rat Brain.

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Department of Anatomy and Cell Biology, University of Western Ontario, London, ON, N6A 5C1, Canada.
Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI, 48201.


Accumulation of beta-amyloid (Aβ) in the brain has been implicated as a major contributor to the cellular pathology and cognitive impairment observed in Alzheimer's disease. Beta-amyloid may exert its toxic effects by increasing reactive oxygen species and neuroinflammation in the brain. This study set out to investigate whether a genetically engineered derivative of the peroxisomal antioxidant enzyme catalase (CAT-SKL), is able to reduce the toxicity induced by intracerebroventricular injection of Aβ25-35 in the mature rat brain. Histopathological and immunohistochemical analyses were used to evaluate neuroinflammation, and neuronal loss. Spatial learning and reference memory was assessed using the Morris water maze. CAT-SKL treatment was able to reduce the pathology induced by Aβ25-35 toxicity by significantly decreasing microglia activation in the basal forebrain and thalamus, and reducing cholinergic loss in the basal forebrain. Aβ25-35 animals showed deficits in long-term reference memory in the Morris water maze, while Aβ25-35 animals treated with CAT-SKL did not demonstrate long-term memory impairments. This preclinical data provides support for the use of CAT-SKL in reducing neuroinflammation and long-term reference memory deficits induced by Aβ25-35.


beta amyloid; catalase; neuroinflammation; oxidative stress

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