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Amarantus BioScience Announces Positive Efficacy Data For MANF In A Nigral Delivery Neurorestoration Animal Model Of Parkinson's Disease

Stocks in this article: AMBS

SUNNYVALE, Calif., Jan. 9, 2013 /PRNewswire/ -- Amarantus BioScience, Inc. (OTCQB: AMBS), a biotechnology company discovering and developing treatments and diagnostics for diseases associated with protein misfolding and apoptosis centered around its patented therapeutic protein Mesencephalic Astrocyte-derived Neurotrophic Factor (MANF), today presented positive preclinical efficacy data for MANF in a neurorestoration 6-hydroxydopamine (6-OHDA) rat model of Parkinson's disease.  The data demonstrate that unlike Glial cell-Derived Neurotrophic Factor (GDNF), MANF significantly reduces behavioral deficits, increases dopaminergic (DA) nerve terminal reinnervation of the striatum, and increases dopamine concentrations in the striatum when MANF is administered directly to the substantia nigra (SNc).  GDNF is an agent currently in clinical trials for Parkinson's disease. Dr. John W. Commissiong, Chief Scientific Officer of Amarantus, presented the data at the OneMedForum 2013 conference on January 8, 2013. The webcast is available online at http://www.onemedplace.com/database/list/cid/13336/.

"Today's data support previously reported behavioral data where MANF demonstrated superiority over GDNF," said Dr. John W. Commissiong.  "Going forward, the Company is in a strong position to advance MANF as a potential disease-modifying treatment for Parkinson's based on unique behavioral, morphological and neurochemical data in standard animal models of the disease." 

In humans and animals, dopamine is a chemical released by DA neurons to send signals to other neurons, and is known as a neurotransmitter. DA neurons are the cells responsible for releasing dopamine, and degenerate in the SNc of Parkinson's disease patients. This degeneration causes DA nerve terminals from the striatum to retract towards their cells bodies in the SNc. The loss of DA nerve terminals in the striatum leads to reduced dopamine levels in the striatum. Therefore, drug treatment to the SNc that increases innervation of the striatum is critical as a basis for functional recovery in Parkinson's disease.

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