Neuroaid - MLC 901, A Traditional Chinese Medicine Induces Neuroprotective and Neuroregenerative Benefits After Traumatic Brain Injury in Rats

I don't have a good enough scientific background to see if this research is valid and reverses the previous negative results for stroke.

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Neuroaid - It’s sold in 25 countries and 20,000 people have taken it, but herbal remedy proves no better than placebo in trial

Chinese herbal remedy for stoke[sic] recovery no better than placebo

CAM taking advantage of stroke patients 

Neuroaid and stroke rehab 

And Peter Levines' comments on it here: 

Neuroaid: Partial Truth and Petty Theft

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  The TBI Neuroaid result here:

Neuroaid - MLC 901, A Traditional Chinese Medicine Induces Neuroprotective and Neuroregenerative Benefits After Traumatic Brain Injury in Rats

• H. Quintard^{a, b},
• T. Lorivel^a,
• C. Gandin^a,
• M. Lazdunski^a,
• C. Heurteaux^{a, ,}

 Show more

DOI: 10.1016/j.neuroscience.2014.06.047

Under a Creative Commons license

  Open Access

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Highlights

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MLC901 prevented the serum increase of two biomarkers S100B and NSE.

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MLC901 reduced the infarct volume up to 2 hours post-TBI.

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MLC901 prevented the edema formation and assists resolution, via the aquaporin 4.

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MLC901 induced an increase of neurogenesis and gliogenesis around the lesion.

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MLC901 reduced cognitive deficits induced by TBI.

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Abstract

Traumatic brain injury is a frequent and clinically highly heterogeneous neurological disorder with large socioeconomic consequences. NeuroAid (MLC601 and MLC901), a Traditional Medicine used in China for patients after stroke has been previously reported to induce neuroprotection and neuroplasticity. This study was designed to evaluate the neuroprotective and neuroregenerative effects of MLC901 in a rat model of traumatic brain injury (TBI). TBI was induced by a moderate lateral fluid percussion applied to the right parietal cortex. MLC901 was injected intraperitoneally at 2 hours post-TBI, and then administered in drinking water at a concentration of 10 mg/ml until sacrifice of the animals. The cognitive deficits induced by TBI were followed by using the “what-where-when” task, which allows the measurement of episodic-like memory. MLC901 treatment decreased brain lesions induced by TBI. It prevented the serum increase of S100B and NSE, which may be markers to predict the neurologic outcome in human patients with TBI. MLC901 reduced the infarct volume when injected up to 2 hours post-TBI, prevented the edema formation and assisted its resolution, probably via the regulation of aquaporin 4. These positive MLC901 effects were associated with an upregulation of VEGF as well as an increase of endogenous hippocampal neurogenesis and gliogenesis around the lesion. Furthermore, MLC901 reduced cognitive deficits induced by TBI. Rats subjected to TBI displayed a suppression of temporal order memory, which was restored by MLC901. This work provides evidence that MLC901 has neuroprotective and neurorestorative actions, which lead to an improvement in the recovery of cognitive functions in a model of traumatic brain injury.