NEW YORK, May 22, 2014 (GLOBE NEWSWIRE) -- Anavex Life Sciences Corp. ("Anavex" or the "Company") (OTCQB:AVXL), a clinical-stage biopharmaceutical company developing novel drug candidates to treat Alzheimer's disease, other diseases of the central nervous system (CNS) and various types of cancer, welcomes new data published in the current issue of The Journal of Neuroscience that has favorable implications for ANAVEX PLUS, the Company's Alzheimer's disease drug candidate combination.
The scientific findings indicate that too much calcium signaling in neurons may be involved in causing Alzheimer's disease (AD). These calcium alterations can be modulated directly through the inositol triphosphate (IP3) receptor, representing a potential new therapeutic approach to treating AD. The findings indirectly confirm the therapeutic opportunity in Alzheimer's disease for ANAVEX PLUS, an agonist of the sigma-1 receptor (S1R), because the S1R acts as a calcium signaling modulator via IP3.
"Since we know from previous data that the sigma-1 receptor is directly involved in regulating intracellular calcium levels, these recent findings provide further confirmation of the potential for our drug candidate combination ANAVEX PLUS, which increases the expression of the sigma-1 receptor," said Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex. "These findings also provide added encouragement for the clinical trial of ANAVEX PLUS, which is scheduled to commence in 2014."
The Journal of Neuroscience report confirms that while normal calcium release is important for synaptic transmission and plasticity, too much is toxic. For the first time, by using a genetic approach, the authors showed that exaggerated neuronal calcium signaling can be normalized by decreasing the expression of IP3 protein by 50%. Importantly, this signaling modulation corrected significantly AD-like biochemical, electrophysiological and behavioral impairments observed in two different early and late-stage AD mouse models. The results indicate that the correction of exaggerated calcium signaling rescues the constitutive activation of this transcriptional pathway and dramatically reduces both hippocampal and cortical Amyloid-beta (Abeta) accumulation and hippocampal tau pathology, both hallmarks of AD.
Compelling evidence suggests that the changes in calcium signaling happen in the absence of or precede the appearance of Abeta plaques, indicating that it is an early event that could be a causative trigger of Alzheimer's disease.
According to the newly published report, the enhanced calcium release constitutes a good approximation event in vivo that contributes both to mild cognitive-like impairments and AD-like impairments in the respective animal models. The displayed abnormalities mirror those observed in presymptomatic patients where there is a family link to the disease and in patients suffering from mild cognitive impairment (MCI), a condition that commonly precedes AD.
Therefore, it is possible that environmental influences and genetic susceptibilities that alter calcium signaling play a role in the development of Alzheimer's disease.
The authors conclude that these results suggest that targeting the IP3 signaling pathway could be considered a potential therapeutic strategy for patients harboring mutations linked to AD.
The report, entitled "Suppression of InsP3 Receptor-Mediated Ca2+ Signaling Alleviates Mutant Presenilin-Linked Familial Alzheimer's Disease Pathogenesis," was authored by Dr. Kevin Foskett and colleagues of the Perelman School of Medicine at the University of Pennsylvania in Philadelphia.
About ANAVEX PLUS
ANAVEX PLUS is a "cocktail" of ANAVEX 2-73 and donepezil (Aricept®). ANAVEX 2-73 is an orally available small molecule with multiple modes of action that holds potential to be disease modifying in Alzheimer's disease. In several Alzheimer's disease models including Tg2576, ANAVEX 2-73 has shown a reversal of memory loss and neuroprotection. Studies with ANAVEX 2-73 have shown a clear synergistic memory effect of up to 80% in combination with donepezil, and up to 7 points cognition improvement in ADAS-Cog at 12 weeks and 5.5 points at 26 weeks in a human calibrated realistic cortical network computer model. Anavex has filed a patent application for the combination of ANAVEX 2-73 and donepezil.
About Anavex Life Sciences Corp.
Anavex Life Sciences Corp. (www.anavex.com) is a clinical-stage biopharmaceutical company engaged in the development of novel drug candidates to treat Alzheimer's disease, other CNS diseases and various types of cancer. ANAVEX 2-73, an orally available drug candidate developed to treat Alzheimer's disease through potential disease modification, has undergone an initial Phase 1 human clinical trial and was well tolerated in doses up to 55mg. Results from preclinical studies indicate that ANAVEX 2-73 demonstrates anti-amnesic and neuroprotective properties. A highly encouraging synergistic effect has also been observed between ANAVEX 2-73 and donepezil (Aricept®). The combined therapeutic, called ANAVEX PLUS, produced up to 80% greater reversal of memory loss in Alzheimer's disease models versus when the drugs were used individually. Anavex is a publicly traded corporation quoted as AVXL.
Forward-Looking Statements
Statements in this press release that are not strictly historical in nature are forward-looking statements. These statements are only predictions based on current information and expectations and involve a number of risks and uncertainties. Actual events or results may differ materially from those projected in any of such statements due to various factors, including the risks set forth in the Company's most recent Annual Report on Form 10-K filed with the SEC. Readers are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. All forward-looking statements are qualified in their entirety by this cautionary statement and Anavex Life Sciences Corp. undertakes no obligation to revise or update this press release to reflect events or circumstances after the date hereof.