Journal
BRAIN PATHOLOGY
Volume 27, Issue 1, Pages 86-94Publisher
WILEY-BLACKWELL
DOI: 10.1111/bpa.12368
Keywords
beta amyloid; catalase; neuroinflammation; oxidative stress
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Funding
- Canadian Institutes of Health Research (CIHR) [R1478A47]
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Accumulation of beta-amyloid (A) 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 A(25-35) 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 A(25-35) toxicity by significantly decreasing microglia activation in the basal forebrain and thalamus, and reducing cholinergic loss in the basal forebrain. A(25-35) animals showed deficits in long-term reference memory in the Morris water maze, while A(25-35) 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 A(25-35.
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