Abstract: Engineered tissue compositions for supporting cell growth, maintenance, and/or differentiation featuring a scaffold, including a dual fiber scaffold, extracellular matrix (ECM) material, and optionally a population of ECM-generating cells such as fibroblasts. The tissue compositions may be used for supporting seeded cells of a particular cell type of interest such as cells related to skeletal muscle, smooth muscle, cardiac tissue, gastrointestinal tissue, etc. The tissue compositions with seeded cells may develop into functional tissues, which may have the potential to provide a tissue graft for therapeutic purposes or a valuable model for in vitro assays.

Abstract: Engineered tissue compositions for supporting cell growth, maintenance, and/or differentiation featuring a scaffold, extracellular matrix (ECM) material, and optionally a population of ECM-generating cells such as fibroblasts. The tissue compositions may be used for supporting seeded cells of a particular cell type of interest such as cells related to skeletal muscle, smooth muscle, cardiac tissue, gastrointestinal tissue, etc. The tissue compositions with seeded cells may develop into functional tissues, which may have the potential to provide a tissue graft for therapeutic purposes or a valuable model for in vitro assays.

Abstract: The present invention provides compositions and methods for improving cardiac function. Specifically, the present invention provides compositions and methods for treating a subject having a disorder or condition associated with aberrant cardiac tissue function, comprising contacting a patient having a disorder or condition associated with aberrant cardiac tissue function with a construct, or a construct associated with therapeutic cells, or a construct associated with fibroblast cells and therapeutic cells.

Abstract: A chimeric non-human mammal disease model, wherein (1) at least 30% of all the glial cells in the corpus callosum of the chimeric non-human mammal are human glial cells, and/or (2) at least 5% of all of the glial cells in the white matter of the brain and/or brain stem of the chimeric non-human mammal are human glial cells, and wherein the human glial cells comprise a combination of a first group of human glial cells tagged with a first label and a second group of human glial cells tagged with a second label that is distinguishable from the first label.

Abstract: The present disclosure is directed to a method of treating a neuropsychiatric disorder. This method involves selecting a subject having the neuropsychiatric disorder and administering to the selected subject a preparation of glial progenitor cells at a dosage effective to treat the neuropsychiatric disorder in the subject. Another aspect of the disclosure is directed to a method of treating a neuropsychiatric disorder that includes selecting a subject having the neuropsychiatric disorder and administering, to the selected subject, a potassium (K+) channel activator at a dosage effective to restore normal brain interstitial glial K+ levels in the selected subject and treat the neuropsychiatric disorder is also disclosed.

Abstract: The present application relates to alleviating adverse effects of oligodendrocyte loss, astrocyte loss, or white matter loss, including age-related oligodendrocyte loss, age-related astrocyte loss, or age-related white matter loss, in the brain of a subject. The present application also relates to rejuvenating a glial progenitor cell or a progeny thereof, or to enhancing the development potential of a glial progenitor cell or a progeny thereof.

Abstract: The present application relates to a method of treating a subject having a condition mediated by a deficiency in myelin. This method involves selecting a subject having a condition mediated by a deficiency in myelin and expressing a transcription factor 7-like 2 (TCF7L2) protein in the selected subject under conditions effective to treat the condition. Also disclosed is a method of increasing oligodendrocyte production from glial progenitor cells. This method involves providing a population of glial progenitor cells and expressing a TCF7L2 protein in the provided population of glial progenitor cells under conditions effective to increase oligodendrocyte production compared to oligodendrocyte production absent said administering. Also disclosed is a genetic construct suitable, inter alia, for carrying out these methods.

Abstract: The present disclosure is directed to systems for in vivo tracking of target cells resulting from implantation of a preparation of cells. The present disclosure is further directed to in vivo methods of tracking a preparation of cells implanted in a subject, and of preparations of cells.

Abstract: The present application relates to alleviating adverse effects of oligodendrocyte loss, astrocyte loss, or white matter loss, including age-related oligodendrocyte loss, age-related astrocyte loss, or age-related white matter loss, in the brain of a subject. The present application also relates to rejuvenating a glial progenitor cell or a progeny thereof, or to enhancing the development potential of a glial progenitor cell or a progeny thereof.

Abstract: A method for rejuvenating glial progenitor cells and rejuvenated glial progenitor cells rejuvenated by such method are disclosed. The method comprises introducing a population of genetically modified glial progenitor cells into the brain and/or brain stem of a subject, wherein the genetically modified glial progenitor cells have increased expression of one or more genes compared to the same type of glial progenitor cells that have not been genetically modified, and wherein the one or more genes are selected from the group consisting of ARX, CEBPZ, DLX1, DLX2, ELK1, ETS1, ETV4, KLF16, MYBL2, MYC, NFYB, POU3F1, SMAD1, SOX3, SP5, TCF12, TFDP1, TP53, ZIC3 and ZNF195.

Abstract: The present disclosure is directed to methods of inducing rejuvenation in a population of adult glial progenitor cells, and methods of treating a subject having a myelin deficiency. The method of inducing rejuvenation in a population of adult glial progenitor cells, may comprise: administering, to the population of adult glial progenitor cells, one or more nucleic acid molecules encoding microRNAs, wherein administering suppresses the signal transducer and activator of transcription 3 (STAT3) signaling pathway; and/or administering microRNAs, wherein administering suppresses the E2F transcription factor 6 (E2F6) signaling pathway; and/or administering microRNAs, wherein administering suppresses the Myc-associated factor X (MAX) signaling pathway, wherein said one or more nucleic acid molecules are administered in an amount sufficient to induce rejuvenation in the population of adult glial progenitor cells.

Abstract: The present disclosure is directed to a method of treating a neuropsychiatric disorder. This method involves selecting a subject having the neuropsychiatric disorder and administering to the selected subject a preparation of glial progenitor cells at a dosage effective to treat the neuropsychiatric disorder in the subject. Another aspect of the disclosure is directed to a method of treating a neuropsychiatric disorder that includes selecting a subject having the neuropsychiatric disorder and administering, to the selected subject, a potassium (K+) channel activator at a dosage effective to restore normal brain interstitial glial K+ levels in the selected subject and treat the neuropsychiatric disorder is also disclosed.

Abstract: The present disclosure is directed to methods of inducing rejuvenation in a population of adult glial progenitor cells, and methods of treating a subject having a myelin deficiency. The method of treating a subject having a myelin deficiency, may comprise expressing, in glial progenitor cells of the subject, one or more transcription factors selected from the group consisting of B-cell lymphoma/leukemia 11A (BCL11A), histone deacetylase 2 (HDAC2), histone-lysine N-methyltransferase EZH2 (EZH2), myc proto-oncogene protein (MYC), high mobility group protein HMGI-C (HMGA2), nuclear factor 1 B-type (NFIB), and transcriptional enhancer factor TEF-4 10 (TEAD2), wherein said expressing is effective to induce myelination in the subject, thereby treating the myelin deficiency.

Abstract: The present application relates to a non-human mammal model of a human neurodegenerative disorder, methods of producing the non-human mammal model, and methods of using the non-human mammal model to identify agents suitable for treating a neurodegenerative disorder. The present application also relates to methods of treating neurodegenerative disorders and restoring normal brain interstitial potassium levels.

Abstract: A genetically modified glial cells, and use of such cells for rejuvenating glial cell population or treating glial cell-related disorders are disclosed. A method of treating a disorder of the brain and/or brain stem in a subject by introducing a population of genetically modified glial progenitor cells into the brain and/or brain stem of the subject, wherein the genetically modified glial progenitor cells have increased expression of one or more genes compared to the same type of glial progenitor cells that have not been genetically modified, wherein said increased expression of the one or more genes in the genetically modified glial progenitor cells confer competitive advantage over native or already resident glial progenitor cells in the subject.

Abstract: The present disclosure is directed to methods of inducing rejuvenation in a population of adult glial progenitor cells, and methods of treating a subject having a myelin deficiency. The method of inducing rejuvenation in a population of adult glial progenitor cells may comprise administering, to the population of adult glial progenitor cells, an effective amount of an agent that suppresses one or more transcription factors selected from the group consisting of (i) zinc finger protein 274 (ZNF274), (ii) Myc-associated factor X (MAX), (iii) E2F transcription factor 6 (E2F6), (iv) zinc finger protein Aiolos (IKZF3), and (v) signal transducer and activator of transcription 3 (STAT3).

Abstract: The present application relates to a non-human mammal model of a human neurodegenerative disorder, methods of producing the non-human mammal model, and methods of using the non-human mammal model to identify agents suitable for treating a neurodegenerative disorder. The present application also relates to methods of treating neurodegenerative disorders and restoring normal brain interstitial potassium levels.

Abstract: The present disclosure relates to methods of treating a human subject having a condition mediated by a deficiency in myelin and methods of increasing oligodendrocyte production from human glial progenitor cells. These methods involve selecting a human subject having a condition mediated by a deficiency in myelin or providing a population of human glial progenitor cells and administering to the subject or the population of human glial progenitor cells one or modulators of a cell signaling pathway selected from the group consisting of Notch signaling, cAMP signaling, CIP2A signaling, RXRA signaling, TCF7L2 signaling, and combinations thereof under conditions effective to treat the condition or increase oligodendrocyte production.

Abstract: The present disclosure relates to a preparation of CD140a/PDGFR? positive cells that comprises oligodendrocyte progenitor cells co-expressing OLIG2 and CD140a/PDGFR?. The preparation of cells is derived from pluripotent cells that were derived from skin cells, fibroblasts, umbilical cord blood, peripheral blood, bone marrow, or other somatic cells. The cell preparation has an in vivo myelination efficiency that is equal to or greater than the in vivo myelination efficiency of a preparation of A2B5+/PSA-NCAM-sorted fetal human tissue derived oligodendrocyte progenitor cells. Methods of making, isolating and using the disclosed cell preparation are also described.

Abstract: This invention relates to improving delivery of agents (e.g., one or more nanoparticles) to the central nervous system.