Amarantus Subsidiary MANF Therapeutics Announces P
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Posted On: 01/29/2018 9:17:29 AM
Amarantus Subsidiary MANF Therapeutics Announces Positive Independent Peer-Reviewed Pre-Clinical Data for MANF in Parkinson’s Disease
Data show in-animal increases in free-release dopamine and dopamine turnover
January 29, 2018 09:00 ET | Source: Amarantus Bioscience Holdings, Inc.
SAN FRANCISCO, Jan. 29, 2018 (GLOBE NEWSWIRE) -- Via OTC PR Wire -- Amarantus Bioscience Holdings, Inc. (OTCPK:AMBS), a US-based biotechnology holding company with wholly-owned subsidiaries developing first-in-class orphan neurologic, regenerative medicine and ophthalmic therapies, today disclosed that its wholly-owned subsidiary MANF Therapeutics announced the publication of an independent peer-reviewed article entitled “Mesencephalic Astrocyte-Derived Neurotrophic Factor (MANF) Elevates Stimulus-Evoked Release of Dopamine in Freely-Moving Rats” in the scientific journal Molecular Neurobiology. MANF is in pre-clinical development for the treatment of orphan ophthalmological disorders, Glaucoma and Parkinson’s disease.
The published data show that 1 week after MANF treatment, there is an increased release of dopamine, as well as increased dopamine turnover, in the rat striatum in response to stimulus, as measured by brain microdialysis. These data are significant because they propose a unique mechanism of action for MANF in Parkinson’s disease that provides a rationale for potentially improved treatment efficacy with MANF versus other neurotrophic factors in-development. Currently-approved drugs for Parkinson’s disease primarily target dopamine replacement as their mechanism of action. Disease-modifying drugs, such as neurotrophic factors, primarily target the rescue of the dopaminergic neurons that degenerate in Parkinson’s disease. A treatment that could both rescue dopaminergic neurons and increase dopamine release could be a significant improvement over other approaches in treating Parkinson’s disease.
A link to the abstract is available here: https://link.springer.com/article/10.1007%2Fs...018-0872-8
https://globenewswire.com/news-release/2018/0...sease.html
Data show in-animal increases in free-release dopamine and dopamine turnover
January 29, 2018 09:00 ET | Source: Amarantus Bioscience Holdings, Inc.
SAN FRANCISCO, Jan. 29, 2018 (GLOBE NEWSWIRE) -- Via OTC PR Wire -- Amarantus Bioscience Holdings, Inc. (OTCPK:AMBS), a US-based biotechnology holding company with wholly-owned subsidiaries developing first-in-class orphan neurologic, regenerative medicine and ophthalmic therapies, today disclosed that its wholly-owned subsidiary MANF Therapeutics announced the publication of an independent peer-reviewed article entitled “Mesencephalic Astrocyte-Derived Neurotrophic Factor (MANF) Elevates Stimulus-Evoked Release of Dopamine in Freely-Moving Rats” in the scientific journal Molecular Neurobiology. MANF is in pre-clinical development for the treatment of orphan ophthalmological disorders, Glaucoma and Parkinson’s disease.
The published data show that 1 week after MANF treatment, there is an increased release of dopamine, as well as increased dopamine turnover, in the rat striatum in response to stimulus, as measured by brain microdialysis. These data are significant because they propose a unique mechanism of action for MANF in Parkinson’s disease that provides a rationale for potentially improved treatment efficacy with MANF versus other neurotrophic factors in-development. Currently-approved drugs for Parkinson’s disease primarily target dopamine replacement as their mechanism of action. Disease-modifying drugs, such as neurotrophic factors, primarily target the rescue of the dopaminergic neurons that degenerate in Parkinson’s disease. A treatment that could both rescue dopaminergic neurons and increase dopamine release could be a significant improvement over other approaches in treating Parkinson’s disease.
A link to the abstract is available here: https://link.springer.com/article/10.1007%2Fs...018-0872-8
https://globenewswire.com/news-release/2018/0...sease.html
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