Anavex Life Sciences Corp. ("Anavex" or the "Comp
Post# of 30067
Posted On: 02/25/2015 9:54:17 AM
Anavex Life Sciences Corp. ("Anavex" or the "Company"
(OTCQX: AVXL) is encouraged by the findings of a research report in the current issue of peer-reviewed scientific journal Frontiers in Cellular Neuroscience. Among its conclusions, the report reveals that ANAVEX 2-73 prevents mitochondrial dysfunction and blocks resulting oxidative stress and apoptosis (cell death) in a nontransgenic mouse model of Alzheimer's disease (AD). Mitochondrial damages have been consistently reported as an early cause of AD and appear before amyloid-beta plaques and memory decline in Alzheimer's patients and transgenic mice. Thus, by preserving mitochondrial functionality and reducing other key AD hallmarks, ANAVEX 2-73 has the potential to prevent, stop, slow or reverse the disease, in addition to treating its symptoms.
"We provided clear evidence that the neuroprotective activity of sigma-1 receptor agonists, including the mixed muscarinic ligand/sigma-1 agonist ANAVEX 2-73, involves mitochondrial protection in AD models. Indeed, the drug efficiently protected mitochondria against amyloid-beta caused impairment of mitochondrial respiration, the key energy producing process within the cell," said Tangui Maurice, PhD, one of the study authors and CNRS Research Director, Head of Team 2 'Endogenous Neuroprotection in Neurodegenerative Diseases', at the University of Montpellier and INSERM. "Mitochondrial dysfunction and resulting oxidative stress are critical hallmarks of Alzheimer's disease pathology and believed responsible for increased amyloid-beta production and Tau hyperphosphorylation."
"We are encouraged by this study, which points to the potential ability of ANAVEX 2-73 to not only protect neurons from oxidative stress and amyloid-beta overproduction, which can cause toxicity and follow-on damage, but also the ability to possibly prevent the onset of the disease," said Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex. "Our approach targets Alzheimer's disease further upstream and apparently blocks these disease hallmarks, which may be a more promising approach. Combined with earlier findings that ANAVEX 2-73 restores mitochondrial functionality, this new report strengthens our compound's potential in Alzheimer's disease to also potentially act as a preventative drug."
The report, entitled "Mitochondrial protection by the mixed muscarinic/sigma-1 ligand ANAVEX 2-73, a tetrahydrofuran derivative, in Ab25–35 peptide-injected mice, a nontransgenic Alzheimer's disease model," was jointly conducted by Valentine Lahmy, Romain Long, Didier Morin, Vanessa Villard and Tangui Maurice from the University of Montpellier and INSERM, the University of Paris-Est, Henri Mondor Institute, INSERM and Amylgen. The full paper is available on the Anavex website at http://www.anavex.com/publications/.
(OTCQX: AVXL) is encouraged by the findings of a research report in the current issue of peer-reviewed scientific journal Frontiers in Cellular Neuroscience. Among its conclusions, the report reveals that ANAVEX 2-73 prevents mitochondrial dysfunction and blocks resulting oxidative stress and apoptosis (cell death) in a nontransgenic mouse model of Alzheimer's disease (AD). Mitochondrial damages have been consistently reported as an early cause of AD and appear before amyloid-beta plaques and memory decline in Alzheimer's patients and transgenic mice. Thus, by preserving mitochondrial functionality and reducing other key AD hallmarks, ANAVEX 2-73 has the potential to prevent, stop, slow or reverse the disease, in addition to treating its symptoms. "We provided clear evidence that the neuroprotective activity of sigma-1 receptor agonists, including the mixed muscarinic ligand/sigma-1 agonist ANAVEX 2-73, involves mitochondrial protection in AD models. Indeed, the drug efficiently protected mitochondria against amyloid-beta caused impairment of mitochondrial respiration, the key energy producing process within the cell," said Tangui Maurice, PhD, one of the study authors and CNRS Research Director, Head of Team 2 'Endogenous Neuroprotection in Neurodegenerative Diseases', at the University of Montpellier and INSERM. "Mitochondrial dysfunction and resulting oxidative stress are critical hallmarks of Alzheimer's disease pathology and believed responsible for increased amyloid-beta production and Tau hyperphosphorylation."
"We are encouraged by this study, which points to the potential ability of ANAVEX 2-73 to not only protect neurons from oxidative stress and amyloid-beta overproduction, which can cause toxicity and follow-on damage, but also the ability to possibly prevent the onset of the disease," said Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex. "Our approach targets Alzheimer's disease further upstream and apparently blocks these disease hallmarks, which may be a more promising approach. Combined with earlier findings that ANAVEX 2-73 restores mitochondrial functionality, this new report strengthens our compound's potential in Alzheimer's disease to also potentially act as a preventative drug."
The report, entitled "Mitochondrial protection by the mixed muscarinic/sigma-1 ligand ANAVEX 2-73, a tetrahydrofuran derivative, in Ab25–35 peptide-injected mice, a nontransgenic Alzheimer's disease model," was jointly conducted by Valentine Lahmy, Romain Long, Didier Morin, Vanessa Villard and Tangui Maurice from the University of Montpellier and INSERM, the University of Paris-Est, Henri Mondor Institute, INSERM and Amylgen. The full paper is available on the Anavex website at http://www.anavex.com/publications/.
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