Abstract: Herein is reported a method for the enzymatic preparation/production of an antibody with a modified glycosylation in the Fc-region comprises the steps of incubating an antibody that has a glycosylation in the Fc-region with one or more enzymes for a time sufficient and under conditions suitable to modify the glycosylation of the Fc-region to a defined form, separating in one or more chromatography steps the antibody with a modified glycosylation in the Fc-region from the one or more enzymes and thereby producing the antibody with a modified glycosylation in the Fc-region and one or more recycled enzymes, and repeating the incubating step with the one or more recycled enzymes at least once.

Abstract: The present disclosure provides methods of reducing cardiovascular risk by administration of a PCSK9 inhibitor to patients having a genetic profile associated with response to PCSK9 inhibitor therapy.

Abstract: The present invention features an antibody mimetic, or an antigen binding fragment thereof, that specifically binds to an allosteric site of Aurora A kinase, therapeutic compositions comprising this antibody mimetic, and the use of the monobody to modulate Aurora A kinase for the treatment of cancer.

Abstract: The present invention refers to soluble Neuregulin-1 isoforms representing Posttranslational Neuregulin-1 modifications as medication in cognition-related neurological disorders, in particular schizophrenia, Alzheimer's and Parkinson's diseases.

Abstract: Methods and compositions relating to motor neurons derived from induced pluripotent stem cells of subjects having a neurodegenerative disease, where the motor neurons exhibit phenotypes characteristic of the neurodegenerative disease, are provided herein. In particular, the present invention provides methods for screening putative therapeutic agents and methods for diagnosing living subjects as having a neurodegenerative disease. In addition, the present invention provides therapeutic gene transfer methods for treating or preventing a neurodegenerative disease in a subject in need thereof.

Abstract: In one aspect, antibodies that specifically bind to a human triggering receptor expressed on myeloid cells 2 (TREM2) protein are provided. In some embodiments, the antibody decreases levels of soluble TREM2 (sTREM2). In some embodiments, the antibody enhances TREM2 activity.

Abstract: Enhanced methods for the generation of medial ganglionic eminence (MGE) cells from pluripotent stem cells are provided that involve an additional step of contacting the cells with an activator of FGF8 signaling while differentiating Pax6+ cells progenitor cells into MGE cells with an activator of sonic hedgehog, and optionally a Wnt inhibitor. The activator of FGF8 signaling shifts the differentiation of the population of cells to NKX2.1+ MGE cells, rather than to CopuTFII+ caudal ganglionic eminence (CGE) cells. Methods for treatment of neurological disorders, such as epilepsy, by transplant of MGE cells, or GABAergic interneurons derived from human pluripotent stem cells, into a subject in need of treatment are also provided. Human pluripotent stem cell derived MGE cells when transplanted successfully suppress spontaneous seizures, e.g. in epilepsy.

Abstract: Retinal progenitors and mature photoreceptor cells can be produced by differentiating human embryonic stem cells on a surface having a laminin matrix thereon made of two laminins One laminin is laminin-521, and the other laminin is either laminin-323 or laminin-523. Stem cells plated on this substrate can be differentiated using various cell culture mediums to obtain the retinal progenitors and mature photoreceptor cells.

Abstract: The present invention relates to an isolated antibody or antigen-binding fragment thereof that binds to human A2AP. The isolated antibody or antigen-binding fragment according to the present invention i) cross-reacts with rabbit and/or cynomolgus A2AP, ii) does not inhibit human plasmin activity, and iii) increases plasmin mediated clot lysis in the presence of A2AP.

Abstract: The present invention relates to using monoterpene or sesquiterpene to permeabilize the blood brain barrier.

Abstract: The invention relates to culturing brain endothelial cells, and optionally astrocytes and neurons in a fluidic device under conditions whereby the cells mimic the structure and function of the blood brain barrier. Culture of such cells in a microfluidic device, whether alone or in combination with other cells, drives maturation and/or differentiation further than existing systems.

Abstract: The invention provides antibodies to tau. The antibodies inhibit or delay tau-associated pathologies and associated symptomatic deterioration.

Abstract: The invention relates to compounds, compositions, and methods for derepressing RE1 silencing transcription factor (REST) target genes are provided. In particular, a peptide having the sequence TEDLEPPEPPLPKEN (SEQ. ID NO: 1) and EDLEPPEPPLPK (SEQ. ID NO: 15), or the reversed sequences made of D-amino acids (retro inverted, RI) nekplppeppeldet (SEQ ID NO: 16) and kplppeppelde (SEQ ID NO: 17), are disclosed for inhibiting REST activity. The peptides are useful to treat, prevent, or ameliorate conditions such as traumatic brain injury, epilepsy, dementia, Huntington's Disease (HD), chronic pain, brain cancer (including glioblastoma multiforme), pancreatic cancer; diabetes, and peripheral nerve injury.

Abstract: Human pluripotent stem cells are differentiated in vitro into forebrain subdomain structures, which are then fused to generate an integrated system for use in analysis, screening programs, and the like.

Abstract: The disclosure pertains to N-terminal epitopes identified in A-beta, including conformational epitopes, antibodies thereto and methods of making and using immunogens and antibodies specific thereto.

Abstract: The present disclosure is directed to single domain antibodies that bind to ?-synuclein and the use of these antibodies for the treatment and diagnosis of ?-synucleinopathies The present disclosure is also directed to polynucleotides encoding the ?-synuclein single domain antibodies, therapeutic vectors comprising these polynucleotides and methods of administering these therapeutic vectors for the treatment of ?-synucleinopathies.

Abstract: The invention is directed to compositions and methods for treating or reducing the likelihood of the development of epilepsy in an individual. The method comprises administering to the central nervous system of an individual in need of such treatment a therapeutically effective amount of an agent capable of increasing the expression and/or activity of miR-128.

Abstract: The present invention relates to novel synthetic odorant receptors capable of cell surface localization upon cellular expression. Specifically, the present invention provides synthetic odorant receptors having a consensus amino acid sequence deduced from a plurality of odorant receptors within an odorant receptor family, wherein the consensus amino acid sequence represents the mostly frequently present amino acid residues for each amino acid position deduced from a plurality of odorant receptors within an odorant receptor family. Additionally, the present invention provides methods of use, methods of synthesis, and cell lines expressing one or more of such novel synthetic odorant receptors.

Abstract: Provided herein are methods of treating a subject with hyperammonemia or a urea cycle disorder. The methods comprise administering to a subject in need thereof a therapeutic amount of a glucagon signaling pathway inhibitor, such that ammonia levels are lowered or that amino acid metabolism enzymes are down-regulated, or a condition or disease characterized by hyperammonemia is mediated, or at least one symptom or complication associated with the condition or disease is alleviated or reduced in severity. The glucagon signaling pathway inhibitor can be a small molecule inhibitor of the signaling pathway, an antisense inhibitor of the signaling pathway, shRNA, siRNA, a GCG neutralizing monoclonal antibody, a GCGR antagonist, a peptide inhibitor of the signaling pathway, a DARPin, a Spiegelmer, an aptamer, engineered Fn type-III domains, etc. The therapeutic methods are useful for treating a human suffering from hyperammonemia or a urea cycle disorder.

Abstract: Disclosed are compositions and methods of treating a neurodegenerative disease in an individual. The methods disclose administration of an Integrin ?4?1, Very Late Antigen-4 positive neural precursor cell (“VLA4+NPC”) transfected with a lentivirus overexpressing wild type GCase to an individual having a neurodegenerative disorder. The neurodegenerative disease may include lipid storage diseases, for example Gaucher disease, Parkinson's disease (PD), Dementia with Lewy bodies.