en Behavioral Neuroscience Behavioral Neuroscience Original Original <div style="text-align: justify;"><span style="font-size:14px;"><span style="font-family:Tahoma;"><span style="line-height:2;"><strong>Introduction</strong>: Alzheimer 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 A&beta; plaques, the build-up of intracellular neurofibrillary tangle (NFT), and neuron loss. Neurotrophic factors play a critical role in the treatment of AD. However, utilizing such neurotrophins has encountered certain difficulties and side effects. Novel technological advancements prioritize innovative dipeptide usage, which offers fewer side effects.&nbsp;<br> <strong>Methods</strong>: The present study endeavors to analyze the compound hexamethylenediamide bis-(N-monosuccinyl-glutamyl-lysine) (lab name: H-MGL), a newly discovered neurotrophin mimetic dipeptide, to alleviate memory impairment in an intracerebroventricular single dose streptozotocin (STZ)-induced Alzheimer model in rats. We arranged 4 groups: Sham and groups receiving STZ and STZ + H-MGL (1 and 2 mg/kg). The H-MGL was administered consecutively for 14 days following the STZ injection. Then, the Morris water maze test was performed.<br> <strong>Results</strong>: The findings suggest that administration of STZ caused a significantly increment in mean escape latency and mean traveled distance in acquisition days. H-MGL at a 1 mg/kg dosage failed to yield any notable improvement in rats compared to STZ. By contrast, 2 mg/kg of H-MGL dosage led to a significant decrease in the latency to first platform crossing and frequency of platform crossings.&nbsp;<br> <strong>Conclusion</strong>: Consequently, the findings above have engendered the notion that H-MGL partially ameliorates cognitive impairment, so it may hold promise for having low side effects to alleviate cognitive deficits in AD or potentially decrease the symptoms associated with its progression.</span></span></span></div> Alzheimer disease (AD), Dipeptide, hexamethylenediamide bis-(N-monosuccinyl-glutamyl-lysine) (H-MGL), Escape latency, Latency to first 583 594 http://bcn.iums.ac.ir/browse.php?a_code=A-10-401-3&slc_lang=en&sid=1 Sarieh Ghasempour srh.ghasempour@gmail.com 13700319475328460050655 13700319475328460050655 No Department of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Nader Maghsoudi maghsudi@yahoo.com 13700319475328460050656 13700319475328460050656 No Neurobiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Homa Manaheji hshardinmanaheji@yahoo.com 13700319475328460050657 13700319475328460050657 No Department of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Rasoul Ghasemi r_ghasemi60@yahoo.com 13700319475328460050658 13700319475328460050658 No Department of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Ali Jaafarisuha ali_jaafari_s@yahoo.com 13700319475328460050659 0009-0005-7170-9804 No Department of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Jalal Zaringhalam jzaringhalam@yahoo.com 13700319475328460050660 13700319475328460050660 Yes Department of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.