Generation of Oligodendrocytes and Establishment of an All-Human Myelinating Platform From Human Pluripotent Stem Cells

Investigators describe a method to generate oligodendrocyte precursor cells from human pluripotent stem cells in only ~20 d, which could subsequently myelinate neurons, both in vitro and in vivo.
[Nature Protocols]
García-León, J. A., García-Díaz, B., Eggermont, K., Cáceres-Palomo, L., Neyrinck, K., Madeiro da Costa, R., Dávila, J. C., Baron-Van Evercooren, A., Gutiérrez, A., & Verfaillie, C. M. (2020). Generation of oligodendrocytes and establishment of an all-human myelinating platform from human pluripotent stem cells. Nature Protocols, 1–29. https://doi.org/10.1038/s41596-020-0395-4 Cite
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Generation of Oligodendrocytes and Establishment of an All-Human Myelinating Platform From Human Pluripotent Stem Cells

Researchers describe a method to generate oligodendrocyte precursor cells from human pluripotent stem cells in only ~20 days, which could subsequently myelinate neurons, both in vitro and in vivo.
[Nature Protocols]
García-León, J. A., García-Díaz, B., Eggermont, K., Cáceres-Palomo, L., Neyrinck, K., Madeiro da Costa, R., Dávila, J. C., Baron-Van Evercooren, A., Gutiérrez, A., & Verfaillie, C. M. (2020). Generation of oligodendrocytes and establishment of an all-human myelinating platform from human pluripotent stem cells. Nature Protocols, 1–29. https://doi.org/10.1038/s41596-020-0395-4 Cite
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Catalent and BrainStorm Cell Therapeutics Announce Partnership for the Manufacture of Mesenchymal Stem Cell Platform Therapy NurOwn®

Catalent and BrainStorm Cell Therapeutics, Inc announced an agreement for the manufacture of NurOwn®, BrainStorm’s autologous cellular therapy being investigated for the treatment of ALS, also known as Lou Gehrig’s disease or motor neuron disease.
[Catalent]
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Prevention of Mitochondrial Impairment by Inhibition of Protein Phosphatase 1 Activity in Amyotrophic Lateral Sclerosis

Scientists found that Dynamin-related protein 1 was dephosphorylated in several ALS models, including those with SOD1 and TDP-43 mutations, and the dephosphorylation was mediated by the pathological induction of protein phosphatase 1 activity in these models.
[Cell Death & Disease]
Choi, S. Y., Lee, J.-H., Chung, A.-Y., Jo, Y., Shin, J., Park, H.-C., Kim, H., Lopez-Gonzalez, R., Ryu, J. R., & Sun, W. (2020). Prevention of mitochondrial impairment by inhibition of protein phosphatase 1 activity in amyotrophic lateral sclerosis. Cell Death & Disease, 11(10), 1–15. https://doi.org/10.1038/s41419-020-03102-8 Cite
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The Peptidyl-prolyl Isomerase Pin1 in Neuronal Signaling: from Neurodevelopment to Neurodegeneration

A highly pleiotropic and context-dependent nature of Pin1 functional activity, strictly dependent on the phosphorylation patterns of its cellular targets, clearly emerges. In the nervous system, Pin1 is fundamental both for embryonic development and cellular homeostasis in adult neurons, due to its role as regulator of cell death and survival.
[Molecular Neurobiology]
Fagiani, F., Govoni, S., Racchi, M., & Lanni, C. (2020). The Peptidyl-prolyl Isomerase Pin1 in Neuronal Signaling: from Neurodevelopment to Neurodegeneration. Molecular Neurobiology. https://doi.org/10.1007/s12035-020-02179-8 Cite
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Therapeutic Benefit of Muse Cells in a Mouse Model of Amyotrophic Lateral Sclerosis

Researchers suggested that Muse cells homed in a lesion site-dependent manner and protected the spinal cord against motor neuron death. Muse cells might also be a promising cell source for the treatment of amyotrophic lateral sclerosis patients.
[Scientific Reports]
Yamashita, T., Kushida, Y., Wakao, S., Tadokoro, K., Nomura, E., Omote, Y., Takemoto, M., Hishikawa, N., Ohta, Y., Dezawa, M., & Abe, K. (2020). Therapeutic benefit of Muse cells in a mouse model of amyotrophic lateral sclerosis. Scientific Reports, 10(1), 17102. https://doi.org/10.1038/s41598-020-74216-4 Cite
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Aclipse Therapeutics Awarded AUD 1 Million Grant from FightMND

Aclipse Therapeutics Inc. was awarded an AUD 1 million drug development research grant from FightMND, the largest independent funder of amyotrophic lateral sclerosis (ALS) research in Australia. The grant supported the translational development of M102, a drug candidate for the treatment of ALS, also known as motor neuron disease or Lou Gehrig’s disease. M102 showed promise to stop and reverse ALS disease progression, as evidenced by data in preclinical models.
[Aclipse Therapeutics Inc (BusinessWire LLC)]
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Muscular Dystrophy Association Awards 15 Grants Totaling More Than $4 Million for Neuromuscular Disease Research

The Muscular Dystrophy Association (MDA) announced the awarding of 15 new MDA grants totaling more than $4 million toward research focused on a variety of neuromuscular diseases, including Duchenne muscular dystrophy, Charcot-Marie-Tooth disease, Becker’s muscular dystrophy, spinal muscular atrophy, amyotrophic lateral sclerosis, myotonic dystrophy type 1 and facioscapulohumeral muscular dystrophy.
[The Muscular Dystrophy Association]
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Harmony Lost: Cell–Cell Communication at the Neuromuscular Junction in Motor Neuron Disease

Scientists consider the biology of the neuromuscular junction (NMJ) and review emerging lines of investigation that are highlighting the importance of cell-cell interaction at the NMJ in spinal muscular atrophy, X-linked spinal and bulbar muscular atrophy, and amyotrophic lateral sclerosis.
[Trends in Neurosciences]
Gromova, A., & Spada, A. R. L. (2020). Harmony Lost: Cell–Cell Communication at the Neuromuscular Junction in Motor Neuron Disease. Trends in Neurosciences, 43(9), 709–724. https://doi.org/10.1016/j.tins.2020.07.002 Cite
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Functional Skeletal Muscle Model Derived from SOD1-Mutant ALS Patient iPSCs Recapitulates Hallmarks of Disease Progression

Phenotypic amyotrophic lateral sclerosis (ALS) skeletal muscle models were developed from iPSCs derived from healthy individuals and ALS patients harboring mutations in the superoxide dismutase 1 gene.
[Scientific Reports]
Badu-Mensah, A., Guo, X., McAleer, C. W., Rumsey, J. W., & Hickman, J. J. (2020). Functional skeletal muscle model derived from SOD1-mutant ALS patient iPSCs recapitulates hallmarks of disease progression. Scientific Reports, 10(1), 14302. https://doi.org/10.1038/s41598-020-70510-3 Cite
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RNA-Binding Proteins Musashi and Tau Soluble Aggregates Initiate Nuclear Dysfunction

Researchers investigated the expression and cellular localization of Musashi (MSI)1 and MSI2 in the brains tissues of Alzheimer’s disease, amyotrophic lateral sclerosis and frontotemporal dementia.
[Nature Communications]
Montalbano, M., McAllen, S., Puangmalai, N., Sengupta, U., Bhatt, N., Johnson, O. D., Kharas, M. G., & Kayed, R. (2020). RNA-binding proteins Musashi and tau soluble aggregates initiate nuclear dysfunction. Nature Communications, 11(1), 4305. https://doi.org/10.1038/s41467-020-18022-6 Cite
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