Abstract
Alzheimer’s disease (AD) is one of the most serious human, medical, and socioeconomic burdens. Here we tested the hypothesis that a rat model of AD (Samaritan; Taconic Pharmaceuticals, USA) based on the application of amyloid beta42 (Abeta42) and the pro-oxidative substances ferrous sulfate heptahydrate and L-buthionine-(S, R)-sulfoximine, will exhibit cognitive deficits and disruption of the glutamatergic and cholinergic systems in the brain. Behavioral methods included the Morris water maze (MWM; long-term memory version) and the active allothetic place avoidance (AAPA) task (acquisition and reversal), testing spatial memory and different aspects of hippocampal function. Neurochemical methods included testing of the NR1/NR2A/NR2B subunits of NMDA receptors in the frontal cortex and CHT1 transporters in the hippocampus, in both cases in the right and left hemisphere separately. Our results show that Samaritan rats™ exhibit marked impairment in both the MWM and active place avoidance tasks, suggesting a deficit of spatial learning and memory. Moreover, Samaritan rats exhibited significant changes in NR2A expression and CHT1 activity compared to controls rats, mimicking the situation in patients with early stage AD. Taken together, our results corroborate the hypothesis that Samaritan rats are a promising model of AD in its early stages.
Highlights
Alzheimer’s disease (AD) is a serious neuropsychiatric disorder, invariably resulting in the death of the patient, preceded by a slow and excruciating deterioration of memory, cognitive abilities and personality, which constitutes a serious burden for patients and for their relatives and the whole society
Our results show that Samaritan ratsTM exhibit marked impairment in both the Morris water maze (MWM) and active place avoidance tasks, suggesting a deficit of spatial learning and memory
The exact etiology of the disease is not known, it presents with extracellular plaques of amyloid beta (Abeta) peptides and intracellular tangles of protein tau (Reiman, 2014)
Summary
Alzheimer’s disease (AD) is a serious neuropsychiatric disorder, invariably resulting in the death of the patient, preceded by a slow and excruciating deterioration of memory, cognitive abilities and personality, which constitutes a serious burden for patients and for their relatives and the whole society. The exact etiology of the disease is not known, it presents with extracellular plaques of amyloid beta (Abeta) peptides and intracellular tangles of protein tau (Reiman, 2014). Both these factors are suspected to play an important role in disease progression (Spires-Jones and Hyman, 2014). Multiple changes reaching beyond the simple description given above have been detected in AD brain neurochemistry (e.g., Cai and Ratka, 2012). These changes can be studied primarily in animal models and post mortem studies, since the living human brain is barely accessible to biochemical examination
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