Materials and methods for modulating protease activated receptor 1 (PAR1) activity to alter myelination are provided.

The present disclosure relates to AAV vectors, compositions, and methods related to converting glial cells to neurons by the use of a NeuroD1 coding sequence in an AAV vector.

The present disclosure relates to AAV vectors, compositions, and methods related to converting glial cells to neurons by the use of ISL1 and LHX3 coding sequences in an AAV vector.

The present disclosure relates to AAV vectors, compositions, and methods related to converting glial cells to neurons by the use of NeuroD1 and Dlx2 coding sequences in an AAV vector.

The present disclosure relates to AAV vectors, compositions, and methods related to converting glial cells to neurons by the use of a NeuroD1 and either Ascl1, ISL1, or LHX3 coding sequences in an AAV vector.

Provided are methods and compositions from reprogramming human glial cells into human neurons. The reprogramming is achieved using combinations of compounds that can modify signaling via Transforming growth factor beta (TGF-β), Bone morphogenetic protein (BMP), glycogen synthase kinase 3 (GSK-3), and γ-secretase/Notch pathways. The reprogramming is demonstrated using groups of three or four compounds that are chosen from the group thiazovivin, LDN193189, SB431542, TTNPB, CHIR99021, DAPT, VPA, SAG purmorphamine. Reprogramming is demonstrated using the group of LDN193189/CHIR99021/DAPT, the group of B431542/CHIR99021/DAPT, the group of LDN193189/DAPT/SB431542, the group of LDN193189/CHIR99021/SB431542, a three drug combination of SB431542/CHIR99021/DAPT. Reprogramming using functional analogs of the compounds is also provided, as are pharmaceutical formulations that contain the drug combinations.

The present invention generally provides methods and compositions for transdifferentiation of an animal cell from a first non-pluripotent cell fate to a second non-pluripotent cell fate. Also provided are methods and compositions for the transdifferentiation of an animal cell from a non-pluripotent mesodermal, endodermal, or ectodermal cell fate to a different non-pluripotent mesodermal, endodermal, or ectodermal cell fate.

The present disclosure provides a method for treating an inflammatory neurological disease comprising administering a population of cells enriched for STRO-1.sup.+ cells and/or progeny thereof and/or soluble factors derived therefrom.

The present invention provides a method for producing parasympathetic neurons from neural crest cells or autonomic neural progenitor cells derived therefrom, comprising a step of culturing the neural crest cells or autonomic neural progenitor cells derived therefrom in the presence of a cAMP production promoter, a BDNF signaling pathway activator, a GDNF signaling pathway activator, an NGF signaling pathway activator, an NT-3 signaling pathway activator, vitamin C, a protein kinase C activator, and a retinoic acid receptor agonist.

A method for generating a reporter cell line comprises culturing a cell line capable of undergoing two or more consecutive stages of differentiation and performing the targeted insertion of two or more secretable reporter genes into the genome of the cultured cell line to form edited cells. One or more first stage inserted secretable reporter genes are placed under control of promoters for genes canonically expressed during the first stage of differentiation, and one or more second stage inserted secretable reporter genes are placed under control of promoters for genes canonically expressed during the second stage of differentiation but not during the first stage of differentiation. Differentiation of the clonally expanded edited cells is then induced to the first stage of differentiation, thus inducing expression of the first stage inserted secretable reporter genes.