The present invention relates to a composition for preventing or treating neurodegenerative diseases. The pharmaceutical composition of the present invention contains at least two selected from the group consisting of an interleukin 10 (IL-10) protein or a gene encoding the same, a glial cell line-derived neurotrophic factor (GDNF) protein or a gene encoding the same, and a glutamate decarboxylase (GAD) protein or a gene encoding the same. Since the pharmaceutical composition of the present invention exhibits a better effect of alleviating and preventing neurodegenerative diseases by co-administration of active ingredients than upon single administration, the pharmaceutical composition of the present invention can exhibit the same or higher effect only with a low concentration of the active ingredients. Therefore, the pharmaceutical composition of the present invention can be advantageously used for the prevention or treatment of neurodegenerative diseases.

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 present inventors found an inhibitory neuron-specific promoter sequence which, although having a shorter length than the mGAD65 promoter, does not impair any of the promoter activity, specificity for inhibitory neurons, and gene expression efficiency, which is specifically a promoter consisting of DNA having a promoter activity, comprising: a base sequence of a Dlx1 binding site and/or a Dlx2 binding site in a glutamic acid decarboxylase (GAD) promoter; and a base sequence of a region ranging from a 5 end of exon 1 to a transcription start site (TSS) in a glutamic acid decarboxylase (GAD).

The present invention provides a method for treating spasticity in a subject. The method includes direct administration of a herpes simplex virus 1 (HSV-1) vector harboring a glutamic acid decarboxylase (GAD) gene (preferably. GAD67) into one or more dermatomes of the subject.

The invention provides a glutamate decarboxylase mutant with improved pH tolerance and use thereof in synthesis of gamma-aminobutyric acid. The mutant is obtained by mutating glutamate decarboxylase having an amino acid sequence as shown in SEQ ID NO. 3. The enzyme activity of the mutant at pH 6.5 is improved to 178% of the original enzyme (SEQ ID NO. 3). The final yield of 1000 g of substrate fed in batches in a 5 L tank for 12 h is up to 688.13 g/L, which is about 52% higher than the productivity of the original glutamate decarboxylase. The final molar conversion rate can reach 98.2%. The invention not only broadens the enzyme activity of GAD under the optimum pH, but also broadens the enzyme activity of GAD under the neutral pH, and enhances the capability of the GAD to synthesize gamma-aminobutyric acid, and therefore is more suitable for industrial production.

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.

Methods for the fermentative production of O-phosphoserine, cysteate, or taurine in microbes or unicellular organisms that contain a serB mutation that either decreases serB expression, reduces the amount of the serB gene product or results in a serB gene product with low enzymatic activity. Genetic modifications of the O-phosphoserine, cysteate, or taurine and/or substrate biosynthetic pathways in unicellular organisms that include bacteria, algae, microalgae, diatoms, yeast, or fungi are disclosed. Also disclosed are fermentation and processing methods for the production of various O-phosphoserine-, cysteate-, or taurine-containing products and the use of the cells, fermentation broth or extracts that contain O-phosphoserine, cysteate, or taurine to produce products for use in food, feed, beverages, dietary and health supplements, cosmetics, personal care, pharmaceuticals, agricultural production, or surfactants.

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.

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.

The present disclosure is based in part on studies on novel tolerogenic peptides derived from a protein expressed by a pancreatic cell, which have been developed for use in antigen-specific immunotherapy for type 1 diabetes. Disclosed is a tolerogenic peptide capable of binding an MHC class II molecule independent of antigen processing for use in the treatment of type 1 diabetes, wherein the peptide is derived from a protein expressed by a pancreatic cell.