Mitochondrial damages have been consistently reported as an early cause of Alzheimer's disease and appear before amyloid-beta plaques and memory decline in Alzheimer's patients and transgenic mice. If so, by preserving mitochondrial functionality and reducing other key Alzheimer's disease hallmarks, it 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 Alzheimer's disease 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, Ph.D., 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."
Participating were the University of Montpellier and INSERM, the University of Paris-Est, Henri Mondor Institute, INSERM and Amylgen.
Citation: Valentine Lahmy, Romain Long, Didier Morin, Vanessa Villard and Tangui Maurice, “Mitochondrial protection by the mixed muscarinic/sigma-1 ligand ANAVEX2-73, a tetrahydrofuran derivative, in Ab25–35 peptide-injected mice, a nontransgenic Alzheimer’s disease model”,
Frontiers in Cellular Neuroscience, Volume 8, Article 463 January 20, 2015