دوره 8، شماره 1 - ( January & February 2017 -- 1395 )                   جلد 8 شماره 1 صفحات 5-12 | برگشت به فهرست نسخه ها




DOI: 10.15412/J.BCN.03080101
PMID: 28446944
PMCID: PMC5396173

Cited 0 times in PubMed Central

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Khalaji N, Sarkissian J, Chavushyan V, Sarkisian V. Protective Effects of Proline–Rich Peptide in a Rat Model of Alzheimer Disease: An Electrophysiological Study. BCN. 2017; 8 (1) :5-12
URL: http://bcn.iums.ac.ir/article-1-668-fa.html
Protective Effects of Proline–Rich Peptide in a Rat Model of Alzheimer Disease: An Electrophysiological Study. مجله علوم اعصاب پایه و بالینی. 1395; 8 (1) :5-12

URL: http://bcn.iums.ac.ir/article-1-668-fa.html


چکیده:  

Introduction: Alzheimer disease (AD) is the most common form of dementia in the elderly that slowly destroys memory and cognitive functions. The disease has no cure and leads to significant structural and functional brain abnormalities. To facilitate the treatment of this disease, we aimed to investigate proline-rich peptide (PRP-1) action of hypothalamus on hippocampal (HP) neurons and dynamics of their recovery, after intracerebroventricular (ICV) injection of amyloid-β (Aβ).
Methods: Experiments were carried out on 24 adult, male Albino rats (average weight: 230±30 g). The animals were randomly divided into 3 groups (control, Aβ, and Aβ plus PRP-1). Electrophysiological patterns of hippocampal neurons in response to stimulation of entorhinal cortex (EC) with high frequency stimulation (50 Hz) were studied.
Results: It was found that Aβ (25-35) suppresses the electrical activity of hippocampal neurons. The PRP-1 would return this activity to normal levels.
Conclusion: In general, PRP-1 has protective effect against AD-related alterations induced byamyloid peptides. This protective effect is probably due to stimulation of the immune and glia system.

نوع مطالعه: Original | موضوع مقاله: Clinical Neuroscience
دریافت: ۱۳۹۵/۲/۲۴ | پذیرش: ۱۳۹۵/۶/۲۰ | انتشار: ۱۳۹۵/۱۰/۱۲

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