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Mohamed, W.

Publications and source records attributed to Mohamed, W..

2 recordsLinked to original sources

Edible Bird's Nest Enhances Memory and Learning in a Rat Model of Sporadic Alzheimer's Disease

Alzheimers disease (AD) has emerged as a major global health concern, with the glutamate hyperexcitability hypothesis suggesting that synaptic dysfunction and neuronal death are key contributors to cognitive impairments. Despite decades of research, current AD treatments only manage symptoms without offering a cure. This study investigates the potential of edible birds nest (EBN) as a therapeutic intervention for mitigating cognitive decline in a streptozotocin (STZ)-induced model of sporadic AD. Male Sprague-Dawley rats were randomly assigned to seven groups: control, sham, STZ, low EBN (LEBN, 300 mg/kg), medium EBN (MEBN, 600 mg/kg), high EBN (HEBN, 1200 mg/kg), and memantine (MEM, 10 mg/kg). On day 1, rats received a 3 mg/kg intracerebroventricular (ICV) injection of STZ and were allowed a 7-day recovery period. Following recovery, the rats were treated with their respective interventions daily via oral gavage for 21 days. Behavioral performance was assessed using the Open Field (OF), Novel Object Recognition Test (NORT), and Morris Water Maze (MWM). After behavioral testing, animals were euthanized, and hippocampal tissues were processed for Congo red staining, Bielschowsky staining, and immunohistochemistry to evaluate the expression of NR1, NR2A, NR2B, Glial fibrillary acidic protein (GFAP), and excitatory amino acid transporter 2 (EAAT2). STZ-treated rats exhibited significant declines in recognition memory, spatial learning, and increased anxiety in the open field, along with elevated Congo red and Bielschowsky staining, and higher expression of N-Methyl-D-aspartate receptor (NMDAR) subunits (NR1, NR2A, NR2B), GFAP, and EAAT2, indicative of astrogliosis and glutamate excitotoxicity. Treatment with MEBN (600 mg/kg) significantly improved exploratory behavior, memory, and cognition in the ICV-STZ rats. MEBN effectively attenuated cognitive decline and modulated hippocampal markers, yielding results comparable to the positive control, memantine. These findings underscore the potential of EBN as a promising therapeutic approach for AD and highlight the increasing relevance of traditional medicine in the treatment of neurodegenerative diseases.

neuroscience↗

The effects of oral supplementation of Japanese sake yeast on anxiety, depressive-like symptoms, oxidative stress, and BDNF changes in chronically stressed adolescent rats

Chronic stress during the pre-pubertal period has adverse effects in developing neuropsychiatric disorders such as depression and anxiety. The administration of supplements with antioxidant properties may alleviate depression and anxiety behavior. This study investigated the effects of oral supplementation of Japanese sake yeast on anxiety, depressive-like symptoms, oxidative stress, and changes in brain-derived neurotropic factor (BDNF) in adolescence rats subjected to chronic stress. In order to assess the effects of chronic stress, adolescent rats were grouped into one non-stressed control group (non-stress) and four different experimental groups. The other animals were subjected to stress and orally received normal saline (Control-stress), 15 mg/kg yeast (Stress-15), 30 mg/kg yeast (Stress-30) and 45 mg/kg yeast (Stress-45). Anxiety and depression-like behavior, BDNF levels, and oxidative stress markers were evaluated. The rats exposed to stress exhibited anxiogenic and depression-like behavior as well as lower levels of BDNF and higher levels of oxidative markers compared with non-stressed rats (P<0.05). However, the oral supplementation of sake yeast decreased anxiogenic and depression-like behavior and oxidative indices, and also increased BDNF levels compared to stressed rats treated with saline in a dose-dependent manner (P<0.05). In sum, stress caused anxiety and depression behavior, increased oxidative indices, and reduced BDNF levels while sake yeast alleviated adverse effects of stress on anxiety and depression behaviors, decreased oxidative markers, and increased BDNF levels.

neuroscience↗