31 results about "Synaptic protein" patented technology

A molecular construct comprises a donor label, an acceptor label, a linker peptide disposed between the donor and the acceptor, the linker having a cleavage site sequence, and a spacer between at least one of (a) the donor and the cleavage site sequence and (b) the acceptor and the cleavage site sequence. Preferably, the construct is selected from the group consisting of CFP-(SGLRSRA)-SNAP-25-(SNS)-YFP, and CFP-(SGLRSRA)-synaptobrevin-(SNS)-YFP. In preferred embodiments, the linker peptide is a substrate of a botulinum neurotoxin selected from the group consisting of synaptobrevin (VAMP), syntaxin and SNAP-25, or a fragment thereof that can be recognized and cleaved by the botulinum neurotoxin. Advantageously, the spacer increases the electronic coupling between the donor label and the acceptor label relative to a corresponding construct without the spacer.

The instant invention is based, at least in part, on a newly-identified proteasome-independent signaling function of ubiquitinated PSD-95. Mdm2 inhibitors, Mdm4 inhibitors, PSD-95 inhibitors, and/or enantiomers and/or derivatives thereof de-crease endocytosis via preventing PSD-95 ubiquitination, and thereby increase AMPAR, NMDAR, D1 dopamine receptor surface expression in response to a given stimulus (e.g., NMDA, Aβ). Accordingly, the invention provides methods for modulating AM-PARS, NMDARs, or D1 dopamine receptors in a neuronal cell by contacting the neuronal cell with an Mdm2 and/or Mdm4 inhibitor or PSD-95 inhibitor and/or enantiomers and/or derivatives thereof. Mdm2 and/or Mdm4 inhibitors decrease the enzymatic activity of the respective proteins, and/or interactions with their respective substrates. Mdm2 and Mdm4 inhibitors and/or PSD-95 inhibitors of the invention are contemplated for use in the treatment of neurological disorders, neurodevelopmental disorders, and psychiatric disorders. The invention also provides methods to screen for new Mdm2 and Mdm4 inhibitors and PSD-95 inhibitors and/or enantiomers and/or derivatives thereof.

The present invention relates to synaptic protein biomarkers and diagnostic and prognostic methods for Alzheimer's disease and other neurodegenerative disorders. The invention also provides compositions for detecting the synaptic protein biomarkers as well as compositions and methods useful for early diagnosis and/or treatment of Alzheimer's disease and other neurodegenerative disorders. The invention also provides methods for detecting biomarkers in vesicles (e.g., exosomes) isolated from a biological sample.

It has been found that syntaxin binds and regulates the nucleotide binding folds (NBFs) of sulfonylurea receptors (SURs) in a ATP- and ADP-dependent manner. The present invention therefore provides methods for identifying compounds that effect the binding between a syntaxin protein and a NBF1 and/or NBF2 of a sulfonylurea receptor (SUR). Compounds identified using the method of the invention are useful for treating and/or preventing diseases and/or conditions that have, as their underlying basis, a dysregulation of K_AT 191 channels.

Methods are provided for discovery of new lead pharmaceuticals useful for addressing diseases and other problems of hearing. Compounds that modulate PSD-95 induction are discovered via use of the Nrg-1/Eos signaling pathway. Cell based assay systems are particularly described that identify modulation of binding of Nrg-ICD with an Eos binding site. Other features include the promotion and/or inhibition of Nrg-ICD translocation across nuclear membranes.

The invention relates to identification of synaptogyrin-3 as a target for treating or inhibiting progression of tauopathies or symptoms of tauopathies. In particular, synaptogyrin-3 inhibitors for use as a medicament in general, and for treating or inhibiting progression of tauopathies or symptoms of tauopathies are envisaged. The invention further relates to methods for identification of or for screening for inhibitors of synaptogyrin-3.

An RNA interference (RNAi) strategy is provided based on use of artificial microRNA (amiR) to reduce NKCC1 expression. In particular, a method is provided that achieves neuron-specific expression of specific amiR against NKCC1 by using a human Synapsin promoter to drive transgene expression.

The invention provides a drug for treating hypothyroidism. The drug is suitable for being used by a hypothyroidism patient who is exactly diagnosed in clinic and then subjected to levothyroxine sodium treatment for three months, but has no significant neurocognitive impairment improvement effect, and the patient orally takes donepezil hydrochloride tablets with the dosage of 5 mg every day. The drug is donepezil hydrochloride, can enhance function exertion of cholinergic nerves, reversibly inhibit hydrolysis of acetylcholin esterase on acetylcholine, increase the concentration of acetylcholine in the brain and promote recovery of related damaged synaptic proteins such as munc-18 and syt-1 in the brain, is more beneficial for recovery of a neurocognitive function of the patient, overcomes the defect that neurocognitive impairment cannot be completely recovered through traditional levothyroxine sodium replacement treatment and achieves the purpose of better treating the hypothyroidism.

The invention discloses an in-tissue visual proximity marking method. The in-tissue visual proximity marker method comprises the following steps that: (1) a plasmid vector 1 and a plasmid vector 2 are transformed into a to-be-observed tissue, wherein the plasmid vector 1 carries a fusion gene for expressing a target protein and PafA, and the plasmid vector 2 carries a fusion gene for expressing a tag protein and Pup (E); and (2) after the target protein is expressed, a marking result is observed through the tag protein. The PUPIL provided by the method of the invention can be applied to the research of animal in-vivo protein visualization, and can be used for visually marking subcellular localization information of electrical synapse and inhibitory chemical synapse proteins in living tissue neurons.

The invention provides an application of Spag6 in a medicine for treating cerebral arterial thrombosis reperfusion mediated synaptic injury. The constructed Spag6 lentiviral vector verifies that the Spag6 can promote the expression of synaptic protein and relieve encephaledema from the animal level. The compound is expected to become a medicine for clinically treating cerebral arterial thrombosis reperfusion mediated synaptic injury.

This invention provides methods of increasing or enhancing the synthesis and levels of phospholipids, synapses, synaptic proteins, and synaptic membranes by a neural cell or brain cell; methods of treating a subject with a memory disorder, memory impairment, neurological disorder, or brain disease or disorder, comprising administering to the subject a composition comprising an omega-3 fatty acid, an omega-6 fatty acid, uridine, a metabolic precursor thereof, or a combination thereof.

The present invention relates to the field of recombinant viral vectors suitable for in vivo delivery of therapeutic genes. Described is an adeno-associated virus (AAV) vector comprising (i) a human growth hormone intron 3 (hGHi3) sequence, (ii) a synaptic promoter sequence and/or (iii) a granulin precursor 3'untranslated region (UTR) sequence operatively linked to a polynucleotide sequence encoding a polypeptide of interest. Particular uses of such vectors are to enhance the expression of a polypeptide of interest, such as a granulin precursor (PGRN), to treat subjects having gene mutations or intrinsic polypeptide levels below physiologically normal levels.

The invention discloses a recombinant Tau epitope chimeric polymer antigen as well as a preparation method and an application thereof. The invention provides the recombinant Tau epitope chimeric polymer antigen, which is a basic unit of 6 or 12 tandem phosphatase activation domains of Tau protein and two helper T cell epitopes Th. The recombinant 6/12*(Tau2-18-Th) chimeric antigen disclosed by theinvention can generate a high-level Th2 type anti-Tau2-18 antibody after being used for immunizing common and model mice in a low-dose and few-time manner, T cell immune response aiming at Tau2-18 isnot generated, the pathological level of A beta (including soluble oligomers) and Tau (including total Tau and phosphorylated Tau) in the brain of the mouse model is reduced, the related synaptic protein level is increased, and the learning and memory ability is improved. Therefore, a recombinant chimeric epitope vaccine targeting Tau2-18 is a new direction of AD novel vaccine research, which hasgreat potential and application prospect in prevention of Alzheimer's disease.