The present invention provides a therapy for treating neuropathic pain by subpial administration of small quantities of a composition for spinal segment-specific upregulation of GAD65 (glutamatedecarboxylase) gene and VGAT (vesicular GABA transporter) gene, which is effective for induction of nociceptive effects by potentiating release of vesicular GABA from infected dorsal horn neurons into the synaptic cleft.

The present invention relates to methods of promoting growth of pancreatic islet cells, especially beta islet cells. In particular, the invention relates to methods of promoting growth of pancreatic islet cells by administration of HGF-MET agonists, such as MET agonist antibodies or fragments thereof. The invention further relates to HGF-MET agonists, such as MET agonist antibodies or fragments thereof, and pharmaceutical compositions comprising said agonists, for use in methods of the invention.

The present disclosure provides T-cell modulatory multimeric polypeptides (TMMPs) comprising a type 1 diabetes (T1D)-associated peptide epitope, MHC class II polypeptides, and one or more immunomodulatory polypeptides. A TMMP of the present disclosure is useful for modulating activity of a T cell. Thus, the present disclosure provides compositions and methods for modulating the activity of T cells, as well as compositions and methods for treating persons who have T1D.

The present invention relates to novel methods and therapies for treating, preventing or delaying the onset of type 1 diabetes. In one aspect, the invention provides a method of preventing, delaying the onset of, or delaying the progression of, type 1 diabetes (T1D) in an individual, the method comprising providing in the individual an anti-inflammatory compound; and a pancreatic autoantigen or a derivative or variant thereof; thereby preventing, delaying the onset of, or delaying the progression of, T1D in the individual.

The present invention provides a method and a pharmaceutical composition for the treatment of the NDO comprising the viral expression vector carrying a transcription cassette that harbors transgene(s) inhibiting/silencing neurotransmission or synaptic transmission of afferent neurons.

This disclosure provides a number of sequences involved in nitrogen utilization, methods of using such sequences, tobacco plants carrying modifications to such sequences, tobacco plants transgenic for such sequences, and tobacco products made from such plants.

The present disclosure relates to methods of treating at least one symptom of a mental disorder or disease of the central nervous system in a subject by modulating the amount of GABA produced in the subject's gut. The present disclosure also relates to methods of culturing the bacterial strain new bacterial strains. Also disclosed are methods of identifying bacterial strains capable of producing GABA, and engineering strains to produce GABA.

The invention relates to a method for assessing the efficacy of an immunotherapy comprising administration of GAD to a patient, comprising the following steps: measuring at least one of GADA IgG subclass distribution; GADA levels; distribution of cytokines secreted from lymphocytes; and lymphocyte proliferation in presence of GAD or CD3/CD28 beads; in a first blood, plasma or serum sample obtained from said patient at a first point in time and in a second blood, plasma or serum sample obtained from said patient at a later point in time; and comparing the so obtained measurements. The invention also relates to novel administration regimens of GAD in treatment or prevention of type 1 diabetes, that may include administration by injection into a lymph node, oral administration of vitamin D and/or an assessment of efficacy according to the above methodology followed by an adjustment of dosage and/or administration route based on said assessment.

The present invention describes a non-transgenic approach to produce truncated glutamate decarboxylase (GAD) genes and the corresponding truncated gene product in plants. More particularly, the invention relates to the removal of the calcium-calmodulin binding domain (CaM-BD) from plant GADs using site-directed mutagenesis or gene-editing techniques. The removal of the CaM-BD from plant GADS results in an active GAD enzyme that is not regulated by the CaM-BD, which increases gamma aminobutyric acid (GABA) production in plant cells, organs or whole plants. Non-transgenic plants with truncated GAD have agronomic benefits, including increased GABA, biomass, yield, sugar, and tolerance to abiotic and biotic stressors. In addition, GABA from plants could be used as nutraceutical, pharmaceutical, or therapeutic compounds or as a supplement in animal feed or for animal feed or as an enhancer for plant growth or yield.

A method for delivery of a therapeutic agent to a nervous tissue. In particular, a method of delivering a therapeutic agent to a nervous tissue protected by the brain-blood barrier or meninges is disclosed. The method for delivery allows delivery of a therapeutic agent to a nervous tissue with high efficiency. In addition, the delivery method of a therapeutic agent to a nervous tissue is safe since it has lower side effects such as nervous damage than a method of administering a therapeutic agent directly to a nervous tissue.