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JCR 2016
جستجوی مقالات
شنبه 22 آذر 1404
Basic and Clinical Neuroscience
، جلد ۱۵، شماره ۵، صفحات ۰-۰
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
A New Dipeptide H-MGL Partially Ameliorates Memory Impairment in an STZ-Induced Alzheimer Model in Male Rats
چکیده انگلیسی مقاله
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is identified by the gradual decline in memory and cognitive function. It is classified by the deposition of Aβ plaques, the build-up of intracellular neurofibrillary tangle and neuron loss. Neurotrophic factors play critical role in the treatment of Alzheimer's disease. However, the utilization of such neurotrophins has encountered certain difficulties and side effects. Novel technological advancements prioritize innovative dipeptides usage, which offer fewer side effects. The present study endeavors to analyze the compound hexamethylenediamide bis-(N-monosuccinyl-glutamyl-lysine) (Lab name: H-MGL), a newly discovered neurotrophin mimetic dipeptide, with the aim of alleviating memory impairment in an intracerebroventricular single dose streptozotocin (STZ)-induced Alzheimer model in rats. We arranged 4 groups consist of sham, groups receiving STZ and STZ+H-MGL (1 and 2mg/kg). The H-MGL was administered consecutively for 14 days following STZ injection subsequently, the Morris Water Maze test was performed. The findings suggest that administration of STZ caused significantly increment in mean escape latency and mean traveled distance in acquisition days. H-MGL at a dosage of 1mg/kg failed to yield any notable improvement in rats when compared to STZ. By contrast, a dosage of 2mg/kg of H-MGL led to a significant decrease in the latency to first platform crossing and frequency of platform crossings. Consequently, the aforementioned findings have engendered the notion that H-MGL partially ameliorate cognitive impairment so it may hold promise for having low side effects to alleviate cognitive deficits in Alzheimer's disease, or potentially decreases the symptoms associated with its progression.
کلیدواژههای انگلیسی مقاله
Alzheimer Disease, Dipeptide, H-MGL, Escape latency, Latency to first
نویسندگان مقاله
| Sarieh Ghasempour
Physiology Department, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
| Nader Maghsoudi
Neurobiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
| Homa Manaheji
Physiology Department, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
| Rasoul Ghasemi
Physiology Department, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
| Ali Jaafari Suha
Physiology Department, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
| Jala Zaringhalam
Physiology Department, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
نشانی اینترنتی
http://bcn.iums.ac.ir/browse.php?a_code=A-10-401-3&slc_lang=en&sid=1
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کد مقاله (doi)
زبان مقاله منتشر شده
en
موضوعات مقاله منتشر شده
Behavioral Neuroscience
نوع مقاله منتشر شده
Original
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