Abstract: Enhanced methods for the generation of medial ganglionic eminence (MGE) cells from pluripotent stem cells are provided that involve an additional step of contacting the cells with an activator of FGF8 signaling while differentiating Pax6+ cells progenitor cells into MGE cells with an activator of sonic hedgehog, and optionally a Wnt inhibitor. The activator of FGF8 signaling shifts the differentiation of the population of cells to NKX2.1+MGE cells, rather than to CopuTFII+ caudal ganglionic eminence (CGE) cells. Methods for treatment of neurological disorders, such as epilepsy, by transplant of MGE cells, or GABAergic interneurons derived from human pluripotent stem cells, into a subject in need of treatment are also provided. Human pluripotent stem cell derived MGE cells when transplanted successfully suppress spontaneous seizures, e.g. in epilepsy.

Abstract: Enhanced methods for the generation of medial ganglionic eminence (MGE) cells from pluripotent stem cells are provided that involve an additional step of contacting the cells with an activator of FGF8 signaling while differentiating Pax6+ cells progenitor cells into MGE cells with an activator of sonic hedgehog, and optionally a Wnt inhibitor. The activator of FGF8 signaling shifts the differentiation of the population of cells to NKX2.1+ MGE cells, rather than to CopuTFII+ caudal ganglionic eminence (CGE) cells. Methods for treatment of neurological disorders, such as epilepsy, by transplant of MGE cells, or GABAergic interneurons derived from human pluripotent stem cells, into a subject in need of treatment are also provided. Human pluripotent stem cell derived MGE cells when transplanted successfully suppress spontaneous seizures, e.g. in epilepsy.

Abstract: The present disclosure provides populations of synchronized post-mitotic migratory cortical interneurons (cINS) derived from pluripotent stem cells and cell culture methods for generating said populations of cINs. The disclosure also provides efficient methods for cryopreservation of the derived cINs.

Abstract: Provided are methods of isolating a novel cell population of midbrain dopaminergic neuronal progenitor cells derived from stem cells using a novel combination markers. The cell population may be used for cell therapies for the treatment of Parkinson's disease and as substrates in pharmacological assays.

Abstract: Enhanced methods for the generation of medial ganglionic eminence (MGE) cells from pluripotent stem cells are provided that involve an additional step of contacting the cells with an activator of FGF8 signaling while differentiating Pax6? cells progenitor cells into MGE cells with an activator of sonic hedgehog, and optionally a Wnt inhibitor. The activator of FGF8 signaling shifts the differentiation of the population of cells to NKX2.1+MGE cells, rather than to CopuTFII+ caudal ganglionic eminence (CGE) cells. Methods for reatment of neurological disorders, such as epilepsy, by transplant of MGE cells, or GABAergic interneurons derived from human pluripotent stem cells, into a subject in need of treatment are also provided. Human pluripotent stem cell derived MGE cells when transplanted successfully suppress spontaneous seizures, e.g. in epilepsy.

Abstract: Provided are methods of isolating a novel cell population of midbrain dopaminergic neuronal progenitor cells derived from stem cells using a novel combination markers. The cell population may be used for cell therapies for the treatment of Parkinson's disease and as substrates in pharmacological assays.

Abstract: The present invention relates to methods for producing neural cells from progenitor or stem cells by activating both the Wnt1-Lmx1a/Lmx1b and the SHH-FoxA2 signaling pathways by, for example, increasing the biological activity of one or more of Wnt1, Lmx1a, Lmx1b, Otx2 and Pitx3 and one or more of SHH, FoxA2 and Nurr1 in the progenitor or stem cells including embryonic stem cells and iPS cells. Such cells may be used for the treatment of Parkinson's disease. The invention further relates to methods for treating Parkinson's disease by increasing the biological activity of one or more of Wnt1, Lmx1b, Lmx1b, Otx2 and Pitx3 and one or more of SHH, FoxA2 and Nurr1 in the midbrain of a patient. In particular, the biological activity of the proteins can be increased by virtue of a cell penetrating peptide fused to the proteins or by transfecting RNAs encoding the proteins such that the host chromosomal DNAs remain intact.