The present invention is directed to a system including neurons over-expressing UBB+1, organized in a 3-dimensional culture, and method of using same. A process for making the system of the invention is also provided.

The invention relates to a genetically modified mouse comprising a heterozygous mutation of Tardbp (TDP-43) gene in that the Asn at amino acid 390 in TDP-43 is substituted with an amino acid that is different from Asn, wherein the genetically modified mouse exhibits Amyotrophic lateral sclerosis (ALS)-like phenotypes, TDP-43 proteinopathies and/or motor neuron degeneration. The invention also so relates to an isolated spinal cord motor neuron differentiated from an embryonic stem cell (ESC) that is obtained from an offspring of a genetically modified mouse according to the invention. Methods for identifying an agent alleviating and/or suppressing ALS-TDP pathogenesis are also disclosed.

The present invention relates to an in vitro method for identifying a skin wound in an individual as being a non-healing skin wound or healing skin wound, in vitro methods for monitoring the healing of a skin wound in an individual, methods for screening for compounds suitable for modulating skin wound healing, as well as kits related thereto.

Provided are an odorant receptor marker of microglia and a use thereof, and according to the odorant receptor marker of microglia and a use thereof according to one aspect, microglia may be detected by measuring an activity or expression level of a protein of an odorant receptor (OR) Olfr110 or Olfr111, and OR ligands of microglia may be selected using them, and an inhibitor or activator against the interaction between the OR and 2-pentylfuran is effectively used in treatment of a neuroinflammatory disease or meningitis.

A production method for a cerebral organoid having amyloid plaques is provided, the method including a step (a) of forming, in the presence of a SMAD inhibitor, an embryoid body from a pluripotent stem cell having a mutation in an Alzheimer's disease-related gene; a step (b) of embedding the embryoid body after the step (a) in an extracellular matrix and three-dimensionally culturing the embedded embryoid body in the presence of a SMAD inhibitor and a glycogen synthase kinase 3β (GSK3β) inhibitor to form an organoid; and a step (c) of removing the organoid after the step (b) from the extracellular matrix and subjecting the removed organoid to stirring culture in a medium, where at least a part of the step (c) is carried out in the presence of leukemia inhibitory factor (LIF).

The disclosure provides methods for rescuing synaptic defects caused by abnormal MeCP2 expression in a subject in need thereof, comprising administering to the subject therapeutically effective amount(s) of a nootropic agent and/or an alpha-7 nicotinic acetylcholine receptor (α7-nAChR) agonist. The disclosure further provides methods for screening candidate drug candidates in a tiered series of assays and models (neurons, MECP2-mosaic neurospheres, and cortical organoids).

The present disclosure provides cell-based compositions for treating diabetes, methods for identifying cells that preferentially differentiate into endoderm cells, and methods for preparing insulin-producing pancreatic cells, as well as related methods of use for treating diseases related to insulin deficiency.

The present disclosure provides methods and kits for diagnosing and assessing SAGE1-positive disorders, and compositions and methods for treating SAGE1-positive disorders. The present disclosure further provides SAGE1 complexes and methods and composition for inhibiting SAGE1 complexes and treating SAGE1-positive disorders.

The disclosure describes the effects of transcription mediated from a promoter on the transcription mediated by divergently coupled supercoiling-sensitive promoter. Transcription initiated from a promoter inhibits transcription mediated by a specific supercoiling-sensitive promoter that is divergently coupled to the promoter. A gyrase inhibitor relieves this inhibition and substantially increases the transcription mediated by the specific supercoiling-sensitive promoter that is divergently coupled to another promoter. Accordingly, the invention pertains to a method for identifying a compound as a gyrase inhibitor or not a gyrase inhibitor based on differential expression of genes under the control of divergently coupled promoters in the presence of the compound. Another embodiment of the invention provides an assay for identifying one or more compounds from a library of compounds as a gyrase inhibitor. Polynucleotides and cells containing such polynucleotides that are suitable for carrying out the methods described herein are also provided.

The present disclosure provides cell-based compositions for treating diabetes, methods for identifying cells that preferentially differentiate into endoderm cells, and methods for preparing insulin-producing pancreatic cells, as well as related methods of use for treating diseases related to insulin deficiency.