NeuroAiD: Pharmacological Data

  • Neurorestorative properties

NeuroAiD increases Brain Derived Neurotrophic Factor (BDNF) production

Brain Derived Neurotrophic Factor (BDNF) expression level is increased by a 2.5-fold effect after 6 weeks of treatment with NeuroAiD in rodent models (p<0.01).

Heurteaux et al. Cerebrovascular Diseases Suppl 2013

BDNF is a growth factor which regulates neuronal survival and protects neurons from glutamate-induced damages. BDNF also encourages proliferation and differentiation of new neurons.

Heurteaux et al., Neuropharmacology, 2010

NeuroAiD promotes denser neuronal networks

Cell cultures with NeuroAiD vs. neurobasal control solution:

Epifluorescence microscopy confirmed the development of an important axonal and dendritic network.

On day 14, in neuronal cell cultures treated with NeuroAiD, epifluorescence showed a remarkable increase of DCX, GAP43 and Synaptotagmin expressions, providing evidence that NeuroAiD triggers:

– Neurogenesis

– Neurite outgrowth


– Synaptogenesis

NeuroAiD promotes both the development of new synaptic connections and the modification of existing ones, including an increase in the number and length of dendrites and synapses. A 60% increase in the length of the neurite was shown at Day 14 for NeuroAiD group.

Heurteaux et al., Neuropharmacology, 2010

NeuroAiD promotes neuroplasticity and neurogenesis to support stroke recovery.

Heurteaux et al, Neuropharmacology, 2010

– NeuroAiD increases proliferation of neuronal progenitor cells by a significant 3-fold effect (p<0.01) in human stem cells.

– NeuroAiD increases the number of mature neurons by a significant 2.1-fold effect (p<0.01) in animal studies.

– Cell cultures treated with NeuroAiD have denser networks of connections with stronger neurons.

  • Neuroprotective properties

In animal models, NeuroAiD significantly increases cell viability compared to control resulting in better preserved functional activities

All these results are consistent and defined a neuroprotective effect of NeuroAiD:

• A pre-treatment with NeuroAiD in drinking water for 6 weeks reduces infarct volume by 40% (p<0.01).

• A post-treatment with NeuroAiD reduces the infarct volume by 47% compared to control ischemic mice at 3 hours post-ischemia (p<0.001).

• Effect of NeuroAiD on locomotors performance in compared to vehicle is +150% at day 3 (p<0.001).

These results encourages prescribing NeuroAiD as soon as possible after the stroke onset to reduce the subacute neuronal death around the damaged area.

Other results illustrating the neuroprotective effect of NeuroAiDs

NeuroAiD prevents neuronal death induced by oxygen glucose deprivation*(OGD).

Moha Ou Maati H, et al. Neuropharmacology 2012

NeuroAiD attenuates OGD-triggered Ca2+ influx in mature cortical neurons.

Moha Ou Maati H, et al. Neuropharmacology 2012

The neuroprotective effect of NeuroAiD is associated with a large hyperpolarization mediated by activation of KATP channels. This hyperpolarization prevents an overload of calcium and release of glutamate excitotoxicity. It participates to the neuroprotective properties of NeuroAiD.

Moha Ou Maati H, et al. Neuropharmacology 2012

Illustration of neuroprotective effect of NeuroAiD in an animal model of Traumatic Brain Injury:

NeuroAiD prevents edema formation and assists its resolution by modulating Aquaporin-4 expression.

Aquaporin-4 is an assembly of proteins, constituting a channel. It belongs to the Aquaporin family, specialized in water conduction through cell membrane. Among other locations, Aquaporin-4 is expressed in the brain and is involved in edema formation and resolution.

NeuroAiD prevents elevation of poor outcome biomarkers (like S100B and NSE, which are markers detected in the blood when the brain is injured).

*p<0,05 versus sham operated group

#p<0,05 versus control TBI group

Quintard et al, Neuroscience 2014

These effects of NeuroAiD are illustrating its neuroprotective properties evidenced in an animal model of traumatic brain injury and show the potential of the product in these damaging injuries.