Research reportInfluence of N-acetyl cysteine on beta-amyloid-induced Alzheimer's disease in a rat model: A behavioral and electrophysiological study

- N-acetyl cysteine (NAC) administration prevents beta-amyloid peptide (Aβ) induced passive avoidance memory impairment.
- NAC significantly potentiated hippocampal PS amplitude and slope of EPSP following injection of Aβ.
- NAC may be useful to prevent and treat the Alzheimer's disease.

Alzheimer's disease is an age-related neurodegenerative disorder characterized by a progressive decline in cognitive function due to the extracellular accumulation and deposition of beta-amyloid peptide (Aβ). The purpose of this study was to evaluate the protective effect of N-acetyl cysteine (NAC) on learning and memory in an Aβ-induced Alzheimer's disease model in adult male rats, using behavioral and electrophysiological methods Thirty-five rats were divided into five groups: control, sham-operated, Aβ, Aβ+NAC (1-14 days), and Aβ+NAC (14-28 days). Learning and memory were evaluated behaviorally using the passive avoidance test and electrophysiologically by assessing hippocampal long-term potentiation, a cellular mechanism of learning and memory. Intrahippocampal Aβ injections reduced step-through latency in the passive avoidance test, and decreased both the amplitude of hippocampal neuron population spikes and the slope of excitatory postsynaptic potentials, compared to the sham and control groups. Administration of NAC in rats receiving Aβ alleviated the Aβ-induced deficits in comparison to the Aβ-only group. The results of this study suggest that NAC shows potential for treatment of Alzheimer's disease.