Memantine represents a new class of effective therapeutic agents for the symptomatic treatment of moderately severe to severe Alzheimer's disease (AD) with moderate affinity and N- non-competitive methyl-D-aspartate. (NMDA) receptor antagonist with strong voltage dependence and rapid kinetics. Treatment with a high therapeutic dose of memantine 10 mg/kg obviously reduced cisplatin-induced neurobehavioral toxicity. Memantine blocks the pores of the NMDA receptor; the mechanisms by which NMDA antagonists might benefit neurobehavioral protection [19]. One of the serious adverse effects of the anticancer drug cisplatin is its neurotoxicity, which can be evoked by activation of the extracellular apoptosis pathway in cells. Since memantine, a clinically used N-methyl-D-aspartic acid (NMDA) receptor antagonist, exhibits anti-apoptotic action in several models of neuronal cell injury, in this study we evaluated the effect of memantine on the neurobehavioral effect induced by cisplatin in mice. 20].In a well-described rodent model, exposure to cisplatin at 5 to 10 mg/kg/day produced several neurological deficits, including hindlimb foot separation and decreased forelimb grip strength. and posterior, ataxia and skeletal muscle weakness. .Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay Additionally, exposure to chemotherapeutic agents has resulted in central-peripheral neuropathy in humans and in laboratory animals, including rats and monkeys. Memantine treatment significantly improved neurological deficits; this result was in accordance with [14] who reported that memantine significantly attenuated cisplatin-induced peripheral neuropathy in rats, resulting in improved body weight, decreased thermal hyperalgesia, improved motor coordination, increased grip strength, improved nerve conduction velocity and higher antioxidant enzyme activities than in cisplatin-treated rats[23]. Body weight is often the most sensitive indicator of the adverse effects of toxic substances. The study found a decrease in body weight after cisplatin administration, which may be attributed to the direct effect of cisplatin on growth, excessive tissue protein breakdown, or a decrease in plasma and tissue proteins. There is evidence that lack of protection against reactive oxygen species (ROS) and lack of oxidative DNA damage repair play an important role in the progression of neurodegenerative diseases. Extensive research has linked neurodegenerative diseases to an overactive glutamatergic system, which leads to overactivation of NMDA receptors, excessive Ca2+ influx, and eventual cell death. Memantine is a neuroprotective agent capable of inhibiting the pathological characteristics of NMDA receptor activation, and at the same time it allows the necessary physiological and cognitive functions to be kept intact. This drug has been shown to normalize impairments in synaptic plasticity and cognition that typically follow excitotoxic neuronal injury. Neuroprotective drugs like memantine with clinical application in neurological diseases could reduce genomic instability of brain tissue in addition to improvingcognitive functions. Recent studies have demonstrated that memantine reduces neuronal cell damage caused by staurosporine and doxorubicin. Corroborating these studies, memantine at a dose of 3 to 15 mg/kg decreased DNA damage in brain tissue. In this dose range, no stereotypic behavior or toxicity signals were observed, suggesting that the reduction in brain DNA damage may be associated with neuroprotective effects. effects of memantine. The frequency of micronuclei increased, but without statistical significance, suggesting that memantine was unable to induce mutagenicity. In a study using lipopolysaccharide infusion to induce neuroinflammatory damage, it was shown that memantine decreased the likelihood of microglial activation, thereby preventing the appearance of micronuclei. Release of arachidonic acid and pro-inflammatory factors from neurons . Memantine increased brain-derived neurotrophic factor mRNA levels, which may mediate its neuroprotective effects, reversed loss of cell viability, and decreased caspase-3/7 activities and catechol-induced ROS level (a component of cigarette smoke). In the CNS, both in vivo and in vitro, previous studies have indicated that the increase in proinflammatory cytokines can be reduced by NMDAR antagonist. Memantine, a well-characterized NMDAR antagonist, is used to treat dementia and Parkinson's disease in the clinic, and it also protects neurons from certain models of neurological injury such as head trauma, ischemic stroke, Spinal cord ischemia or neuroinflammation. Therefore, in the process of neuroinflammation, glutamate release and NMDAR activation can enhance neuroinflammation and further deteriorate CNS injury. Excessive activation of CNS NMDA receptors induces Ca2+ overload and oxidative stress, leading to neurodegeneration. These observations have spurred the development of several NMDA antagonists, many of which are effective in animal models of neurodegeneration. Memantine can cause almost complete inhibition of NMDA receptors. Memantine blocks the pores of the NMDA receptor. Therefore, synaptic transmission via NMDA receptors is maintained in the presence of memantine. On the other hand, this study suggests the possible usefulness of a pharmacological strategy based on a drug already widely used in the clinic. The availability of drugs that can be used to block NMDA receptors, such as memantine, contrasts with the future promise of gene therapies or other as-yet-unproven strategies that may be needed for some other potential therapeutic targets.[12,34,35] . (6 months) alcohol ingestion led to learning deficits in Morris water maze rats. Treatment with memantine starting at the beginning of the withdrawal phase (bolus of 20 mg/kg followed by 1 mg/kg every 12 h for 4 weeks) resulted in a complete reversal of these behavioral disturbances. Memantine (30 mg/kg/day; po) for 2 to 3 weeks significantly improved acquisition of the water maze task in mice without affecting swimming speed. Memantine enhanced neurogenesis at therapeutically relevant concentrations in cortical cultures in vitro (best effects were observed at 1 µM, with 140% control neurogenesis) and in the subventricular zone of the DG and forebrain in vivo (7.5 mg/kg po once daily for 14 days, approximately 126% of control neurogenesis), in another study, acute treatment of rats receiving memantine (20.