Abstract: The inventors surprisingly found that neural stimulation caused the synthesis and degradation of proteins into peptides which were then secreted into the cell media within minutes of stimulation by a novel neural-specific and membrane bound proteasome (neuronal membrane proteasome or NMP) that is transmembrane in nature. These secreted, activity-induced, proteasomal peptides (SNAPPs) range in size from about 500 Daltons to about 3000 Daltons. Surprisingly none of the peptides appear to be those previously known to have any neuronal function. Moreover, these SNAPPs have stimulatory activity and are heretofore a new class of signaling molecules. Moreover, the NMP appears to play a highly significant role in aspects of neuronal signaling known to be critical for neuronal function.

Abstract: The present invention in various aspects and embodiments provides methods for the treatment or prevention of degenerative disc disease or chronic lower back pain.

Abstract: Methods for ameliorating neurodegenerative disorders and methods for ameliorating inflammatory disorders comprising administering to said subject an effective amount of a polypeptide comprising, in order from N-terminus to C-terminus, R-X1-X2-X3-X4-X5-R? wherein: R is optionally 1-5 additional ?-amino acids of either L-configuration or D configuration; X1 is any amino acid of either L-configuration or D-configuration; X2 is any amino acid of either L-configuration or D-configuration; X3 is Asp or Glu of either L-configuration or D-configuration; X4 is any amino acid of either L-configuration or D-configuration; X5 is any amino acid of either L-configuration or D-configuration; and R? is optionally 1-5 additional ?-amino acids of either L-configuration or D-configuration, with the proviso that at least three of X1, X2, X3, X4, and X5 are of the D-configuration, wherein the N-terminus is optionally modified by acetylation, and wherein the C-terminus is optionally modified by amidation and/or methylation.

Abstract: The present disclosure provides a polypeptide capable of dissolving protein aggregates. Also provided is a method of treating a neurodegeneration disease using the polypeptide.

Abstract: Methods and kits for diagnosing or monitoring systemic lupus erythematosus (SLE) in a subject are provided. Particularly, the present invention relates to a specific antibody reactivity profile useful in diagnosing or monitoring SLE in a subject.

Abstract: The present disclosure is directed to reducing nocturnal voids by administering a dose of desmopressin over a minimum treatment period compared to before administration, and maintaining or improving the reduction of nocturnal voids over the minimum treatment period.

Abstract: The present invention relates to new methods for assessing prognosis of recovery of DILI in a patient, combining measurement of serum markers through a logistic function that doesn't include bilirubin and transaminases (AST and ALT) markers.

Abstract: A method is provided for determining the presence of soluble, misfolded ?-synuclein protein in a biological sample. The method comprises contacting the biological sample with a pre-incubation mixture, the pre-incubation mixture comprising: a monomeric ?-synuclein protein; a buffer composition; a salt; and an indicator, to form an incubation mixture. An incubation cycle is conducted on the incubation mixture in the presence of either a silicon nitride bead or a borosilicate glass bead having a diameter of from about 1 mm to about 5 mm. The method further comprises determining if a detectable amount of misfolded ?-synuclein aggregate is present in the biological sample.

Abstract: The present invention relates to methods for regulating prohormone convertase (PC1) and compounds and treatments which increase PC1 levels, for treating Prader-Willi Syndrome (PWS).

Abstract: In some embodiments herein, methods, compositions, and uses for modulating lymphatic vessels of the central nervous system are described. In some embodiments, methods, compositions, or uses for treating, preventing, or ameliorating symptoms of a neurodegenerative disease comprise by increasing flow via meningeal lymphatic vessels are described. In some embodiments, methods, compositions, or uses for treating, preventing, or ameliorating symptoms of inflammatory neurological disease be inhibiting or preventing immune cell migration through meningeal lymphatic vessels are described.

Abstract: Disclosed herein are methods that aid in the diagnosis and evaluation of a human subject that has sustained or may have sustained an injury to the head, such as mild or a moderate, severe, or moderate to severe traumatic brain injury (TBI), by detecting levels of cardiac troponin I (cTnI) and one or more early biomarkers which are not cTnI, such as ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), glial fibrillary acidic protein (GFAP), or a combination thereof, in biological samples taken from a human subject at time points within about 24 hours of injury after the subject has sustained or may have sustained the injury to the head.

Abstract: The invention includes a chimeric autoantibody receptor (CAAR) specific for anti-muscle-specific kinase (MuSK) B cell receptor (BCR), compositions comprising the CAAR, polynucleotides encoding the CAAR, vectors comprising a polynucleotide encoding the CAAR, and recombinant cells comprising the CAAR.

Abstract: The present invention relates to a pharmaceutical composition for preventing or treating neurodegenerative diseases comprising a COX2 acetylating agent as an active ingredient and, more particularly, to a pharmaceutical composition for preventing or treating neurodegenerative diseases comprising, as an active ingredient, a COX2 acetylating agent which exhibits an effect of inhibiting the deposition of amyloid-? in brain neurons, reducing excessive neuroinflammatory responses, and increasing the phagocytosis of amyloid-? in microglial cells. The pharmaceutical composition for preventing or treating neurodegenerative diseases comprising the COX2 acetylating agent as an active ingredient has the effects of alleviating neuroinflammation by promoting COX2 acetylation in neurons and secreting specialized pro-resolving mediators (SPMs) and thus, can be very useful in the development of a preventive or therapeutic agent for neurodegenerative diseases.

Abstract: The subject invention concerns materials and methods for treating a person or animal having cognitive impairment. In one embodiment, the method comprises administering an effective amount of one or more inflammatory mediator(s), for example, fms-related tyrosine kinase 3 (Flt3) ligand, interleukin-6 (IL-6), macrophage migration inhibitory factor (MIF), interleukin-1 (IL-1), interleukin-3 (IL-3), erythropoietin (EPO), vascular endothelial growth factor A (VEGF-A), hypoxia-inducible transcription factor (HIF-1alpha), insulin like growth factor-1 (IGF-1), tumor necrosis factor (TNF), granulocyte colony-stimulating factor (G-CSF), granulocyte/macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF), Stem Cell Factor (SCF), Darbepoetin (ARANESP), and metalloproteinases, to an animal or person in need of treatment.

Abstract: The present disclosure relates to delta-2-tubulin and its use as a biomarker for determining if a subject is at risk of developing peripheral neuropathy or if a subject has developed peripheral neuropathy. The present disclosure further relates to methods for the treatment of peripheral neuropathy in a subject and assays for identifying compounds that can be used to treat and/or prevent peripheral neuropathy.

Abstract: The present invention provides novel methods of identifying, monitoring or determining the risk of developing a protein misfolding neurodegenerative disorder in a subject, particularly an alpha synucleinopathy (including Parkinson's disease and dementia with Lewy bodies) using extracellular vesicle samples. Corresponding methods for selecting a treatment and assaying for the presence of a pathological prion-like protein (or one or more ceramide species) in an extracellular vesicle sample are also provided.

Abstract: The present invention relates to uses of a peptide comprising an amino acid sequence selected from the group consisting of SEQ ID NO: 1, SEQ ID NO: 2, analogues and derivatives thereof, for the treatment of neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS). The present invention further provides a method for assessing responsiveness to treatment with the peptide of the invention. In addition, the present invention relates to prognosis of ALS progression, using Akt and phosphorylated Akt as biomarkers.

Abstract: Therapeutic peptides of the following sequence are disclosed: Xaa1-Xaa2-Xaa3-Xaa4-Xaa5, and optionally further comprising Xaa6, wherein Xaa represents an amino acid; Xaa3 is proline; and subscripts represent the positions of each amino acid in the peptide sequence starting from the amino terminus of said peptide extending to the C-terminus. A therapeutic peptide optionally includes a linker that cyclizes the peptide. Also described are methods of treating a neurodegenerative disorder and/or injury in a human subject in need of such treatment by administering to the subject a therapeutically effective amount of a therapeutic peptide as disclosed herein.

Abstract: The present invention relates to methods of determining if a subject has an increased risk of suffering from memory impairment. The methods comprise analyzing at least one plasma sample from the subject to determine a value of the subject's metabolite profile and comparing the value of the subject's metabolite profile with the value of a normal metabolite profile. A change in the value of the subject's metabolite profile, over normal values is indicative that the subject has an increased risk of suffering from memory impairment compared to a normal individual.

Abstract: Provided herein are polypeptides that bind to the malodour-causing substance DMTS. Also provided are nucleic acid sequences that encode for the polypeptides. Further provided herein is a method for identifying a compound that binds, suppresses, blocks, inhibits, and/or modulates the activity of one or more olfactory receptor that is activated by the malodor-causing substance DMTS comprising a) contacting the receptor, or a chimera or fragment thereof with a compound and b) determining whether the compound has an effect on the activity of the receptor. Further provided is an expression vector comprising the nucleic acid encoding the polypeptides described as well as a non-human organism or a host cell modified to express a receptor that is activated by DMTS. Also provided is the use of the polypeptides for identifying malodor modulating compounds.