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The paper describes the results of a series of in vivo and in vitro experiments demonstrating the neuroprotective and neuroproliferative effects of NeuroAiD when given prior to and/or after injury in rodent models of ischemic stroke and neuronal injuries, human embryonic stem cells, and neuronal cell cultures. It shows how NeuroAiD supports neuroplasticity by its effect on neurogenesis, neuritic outgrowth, and synaptogenesis. NeuroAiD provides a better milieu for post-stroke recovery and decreases neurological impairments.
The paper describes the results of a series of in vivo experiments demonstrating neuroprotective and neurogenesis effects of MLC901 on hippocampal CA1 region against global ischemia in rodent models of global ischemia. It shows how neuronal protection by MLC901 is likely mediated by the Akt protein (a central mediator in the signal transduction pathway involved in cell survival) and reduction of oxidative stress. MLC901 prevents necrosis and apoptotic cell death induced by global ischemia, enhances neurogenesis, and enhances functional recovery. This makes MLC901 a potential novel therapeutic strategy in treating cognitive and neurological deficits caused by global ischemia from conditions that deprive the brain of oxygen and glucose, such as cardiac arrest.
This paper highlights the potency of NeuroAid in neuroprotection with the discovery of a key underlying mechanism of action. The activation by NeuroAid of the ATP-sensitive potassium channel located in the suffering neurons of the brain protects them from death. Indeed, the opening of the channel decreases the excitability of neurons (by hyperpolarization) preventing an overload of calcium and release of excitotoxic glutamate. Besides the beneficial effects in neuroplasticity already published, these results strengthen the interest of NeuroAid in stroke recovery.
This paper reviews the pharmacological effects of NeuroAiD on the normal and ischemic brain and neurons. In vivo and in vitro experiments using mouse model of stroke (focal ischemia), rat model of cardiac arrest (global ischemia) and cortical neurons in culture were reviewed and summarized. In conclusion NeuroAID demonstrated both neuroprotective and neuroregenerative properties in rodent models of focal and global ischemia and in cortical cell cultures.
This publication is a post-hoc analysis performed on data from subjects included in the Chinese Medicine Neuroaid Efficacy on Stroke recovery (CHIMES) study. The CHIMES study is an academic international double-blind placebo-controlled clinical trial which treated and monitored 1100 patients from several countries who had suffered an ischemic stroke of intermediate severity within 72 hours, for 3 months. Early vascular events were defined as a composite of recurrent stroke, acute coronary syndrome, and vascular death occurring within 3 months of stroke onset. The research concluded that the risk of early vascular events during the 3-month follow-up was significantly reduced by half in the MLC601 group as compared to the placebo group without an increase in nonvascular deaths. Kaplan–Meier survival analysis demonstrated the difference in risk as early as the first 14 days after stroke.
The CHIMES study is an academic international double-blind placebo-controlled clinical trial which treated and monitored 1100 patients from several countries who had suffered an ischemic stroke of intermediate severity within 72 hours, for 3 months. The research concluded that NeuroAiD is statistically no better than placebo in improving outcomes at 3 months when used among patients with acute ischemic stroke of intermediate severity. However the results of the study confirmed the overall benefit of NeuroAiD in stroke recovery and showed that treatment effect for achieving functional independence was greater among non-acute strokes, consistent with previous studies. In addition the study showed that NeuroAiD had an excellent safety profile.
This publication updates the 2-study meta-analysis published in Stroke journal in 2009 with all clinical data available since on NeuroAiD and provides an overall assessment of the effects of NeuroAiD in improving functional and motor outcomes by the end of treatment. In a systematic review this paper shows that previous studies on NeuroAiD in ischemic stroke in general were of low risk of bias. The meta-analysis showed a statistically significant beneficial effect in favor of NeuroAiD on functional outcome when assessed at the end of study treatment. Although the results did not reach statistical significance, the overall effects on motor recovery were also in favor of NeuroAiD.
The paper reports the pooled analysis of two randomized controlled clinical trials (initial stroke trials in China) that included 605 patients recruited between 2 weeks and 6 months after their stroke. The results show that patients on NeuroAiD have 2.4 times more chances of achieving independence after 1 month of treatment, and have a 25% better recovery in motor impairments. No serious adverse event was reported.
This study of 150 Iranian patients with a recent ischemic stroke (within 1 month) shows that MLC601 improves motor recovery as early as 4 weeks and persisted up to 12 weeks after stroke. Moreover, good tolerability to treatment was shown and adverse events were mild and transient. No severe adverse event leading to drug discontinuation was reported.
This randomized double-blind placebo-controlled study recruited 80 patients within 1 week of stroke, of which 40 received 4 capsules of NeuroAiD 3 times a day and 40 others received placebo for 3 months. The subjects were recruited at Ahvaz Golestan Hospital in Iran from April 2009 to March 2010. This study shows that MLC601 improves cerebral blood flow velocity in post-cerebral infarction subjects better than in the control group. This is associated with more improvement in functional outcome (Barthel Index of activities of daily living) as compared to placebo at 3 months.
In the clinic, the natural recovery rate of homonymous hemianopsia caused by occipital lobe infarction is low. This prospective study compared the effects of NeuroAiD (MLC601) versus piracetam in improving visual field defects in 40 patients matched for age and sex within 1 week of PCA infarction with pure homonymous hemianopsia. After 3 months of treatment, the findings suggest that MLC601 is superior to piracetam for reducing quantitative visual field defects in homonymous hemianopsia patients.
This study on 150 patients with acute ischemic stroke within 1 week of onset demonstrates the longterm (up to 6 months) safety of NeuroAiD in a Caucasian population. While mild nausea was more commonly reported in the NeuroAiD group, none of the reported adverse events were serious or required discontinuation of treatment. There was no significant change observed in blood pressure, hematologic, hepatic, and renal functions during treatment with NeuroAid and up to 3 months after completion of a 3-month regimen. These data confirm the excellent safety profile of NeuroAiD in patients with acute ischemic stroke during treatment and long after completion of treatment.
This study on 114 patients with acute ischemic stroke randomized within 48 hours of onset shows that serious adverse events (SAEs) were similar between the group treated with placebo and the group treated with MLC601. The SAEs reported were those commonly seen in stroke patients. There were neither statistically or clinically significant differences between treatment groups in biochemical, haematological, or electrocardiogram tests at 3 months, nor any statistically or clinically significant differences in the absolute and relative changes of the various parameters between baseline and 3 months. Thus, MLC601 is safe for patients with acute stroke receiving a 3-month treatment.
NeuroAiD does not significantly affect hematological, hemostatic, and biochemical parameters in normal and stroke patients. Clinical parameters and expected effects of aspirin are not altered by co-administration of the drug even when started and maintained at the early stage of acute stroke.