Author/Authors :
-، - نويسنده Department of Cellular- Molecular Nutrition, School of Nutrition Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran Alimohammadi-Kamalabadi, Malek , -، - نويسنده Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran Eshraghian, Mohammadreza , -، - نويسنده Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran Zarindast, Mohammad-Reza , -، - نويسنده Anatomy and Cell Biology Department, School of Medicine, Shahid Beheshti University of Medical Sciences Aliaghaei, Abbas , -، - نويسنده Department of Cellular- Molecular Nutrition, School of Nutrition Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran Pishva, Hamideh
Abstract :
Objective(s): Neuroprotective effect of creatine (Cr) against β-amyloid (Aβ) is reported in an in vitro study. This study investigated the effect of Cr supplementation on β-amyloid toxicity in vivo.
Materials and Methods: Thirty two, male Wistar rats were divided into 4 groups. During ten weeks of study, control group went through no surgical or dietary intervention. At the 4th week of study Sham group had a hippocampal normal saline injection, while Aβ and AβCr groups had an β-amyloid injection in the hippocampus. AβCr group were fed by Cr diet during the study. After 10 weeks, Morris water maze (MWM) test was administered to measure learning ability and memory retrieval. Animals were sacrificed for TUNEL anti apoptotic assay and staining of amyloid plaques by Thioflavin-T.
Results: There was a significant retention deficit among AβCr and Aβ group while the escape latency and the distance traveled to the platform were significantly higher in AβCr group compared to Aβ group. AβCr group had same percent of TUNEL positive neurons compared to Aβ group.
Conclusion: Cr supplementation before and after β-amyloid injection into the CA1 area of hippocampus deteriorates the learning and memory impairment of rats and it does not protect neuronal apoptosis caused by β-amyloid.
