The present disclosure provides monoclonal antibodies that selectively bind to pathological tau over native tau. In certain aspects, the antibodies inhibit or minimize propagation of tau aggregates and/or reduce spread of pathological tau in vivo. In other aspects, the disclosure comprises a method of treating, ameliorating, and/or preventing a tauopathy in a subject, comprising administering any one of the antibodies of the disclosure to the subject. In yet other aspects, the disclosure comprises methods of detecting pathological tau using any one of the antibodies of the disclosure.

The present invention relates to a method for producing induced dopaminergic neuronal progenitors from adult cells using direct reprogramming, induced dopaminergic neuronal progenitors produced via the method and a use for same, wherein, as a result of having been directly reprogrammed from adult cells, the induced dopaminergic neuronal progenitors produced by means of the present invention can be transplanted inside a living body without the risk of oncogenicity, and have excellent proliferative capacity and dopaminergic neuronal differentiation potency, thus can be usefully utilized as a cell therapy product for Parkinson's disease.

The present invention relates to antibody-based probes (including single domain antibody fragment, scFv molecules, antibodies, antibody fragments, diabodies, and the epitope-binding domains thereof) that are capable of immunospecifically and selectively binding to a phospho-serine-containing epitope of Tau, such as, for example, Tau-phospho-serine 396/404 peptide. Such imaging ligands are useful to detect pathological Tau protein conformer if present in a biological sample, especially in conjunction with the diagnosis of Alzheimer's disease or other tauopathy, and thus provide a diagnostic for Alzheimer's disease and other Tau pathologies. The scFv molecules of the present invention have utility as diagnostic markers for, Alzheimer's disease and related tauopathies and as pharmaceutical compositions for the treatment of such conditions.

Described herein are compositions and methods for diagnosing late-onset Alzheimer's disease (LOAD), treating LOAD and assessing efficacy of therapeutic agents used to treat LOAD.

A method of attenuating, treating or preventing cognitive aging in an individual who does not have dementia includes administering to the individual a therapeutically effective amount of a composition containing an omega-3 fatty acid, a nitric oxide releasing compound, Vitamin B12 and choline. The composition is administered in a daily dose that provides 0.1 to 50 times the recommended daily requirement (RDA) of Vitamin B12 per day, more preferably 0.1 to 40 times the recommended daily requirement (RDA) of Vitamin B12 per day and 0.01 to 10.0 times the recommended daily requirement (RDA) of choline. Optionally Vitamin B6 and/or Vitamin B9 can be included in the composition. The method can achieve a benefit that is one or more of decreasing brain atrophy, increasing or maintaining number of synapses, increasing amyloid-β phagocytosis, or decreasing or maintaining neuroinflammation in the non-demented individual. The method can prevent dementia in an individual at risk thereof, for example an elderly human.

The disclosure provides biomarkers for diagnosis and monitoring of transthyretin (TTR) amyloidosis. The disclosure further provides methods for selection of agents for treatment of TTR amyloidosis using the biomarkers. The disclosure further provides kits for practicing the methods provided herein.

The invention relates to a method of determining the likelihood of an individual transitioning to a first episode of psychosis (FEP), the method comprising determining the level of selected markers in a bodily fluid sample from the individual, wherein the increase or decrease in the markers is predictive of the individual transitioning to a first episode of psychosis (FEP). The invention also relates to a method of predicting the functional outcome for an individual following a first episode of psychosis (FEP), the method comprising determining the level of selected markers in a bodily fluid sample from the individual, wherein the increase or decrease in the markers is predictive of an increased risk of functional disability outcome for the individual.

The invention relates to an aqueous solution of AuCl.sub.3×2H.sub.2O or HAuCl.sub.4×4H.sub.2O, ZnCl.sub.2 or ZnSO.sub.4, and AgNO.sub.3 having an Au.sup.3+ concentration of 0.8 mM-1.6 mM, a Zn.sup.2+ concentration of 15 μM-50 μM, and an Ag.sup.+ concentration of 5 μM-50 μM. The invention extends to a kit comprising a solution of the invention, a method of preparing said solution, and the use of a solution of the invention, a solution prepared by a method of the invention, or a kit of the invention in predicting and/or diagnosing and/or monitoring a neurocognitive disorder of the Alzheimer's disease spectrum. The invention extends to a method for predicting and/or diagnosing and/or monitoring a neurocognitive disorder of the Alzheimer's disease spectrum in a patient comprising contacting a tear sample from the patient normalised for protein concentration with a solution of the invention; applying an amount of the tear sample thus obtained to a surface; allowing the tear sample to dry; and drawing a conclusion based on the pattern of the thus obtained dried tear sample, whether the patient is at risk of or suffers from a neurocognitive disorder of the Alzheimer's disease spectrum.

The present disclosure provides in one aspect monoclonal antibodies that bind α-Synuclein. In certain aspects, the antibodies preferentially bind to α-Synuclein fibrils over α-Synuclein monomer. In other aspects, the disclosure provides a method of treating, ameliorating, and/or preventing α-Synucleopathic disease in a subject, comprising administering any one of the antibodies of the disclosure to the subject. In yet other aspects, the disclosure provides methods of detecting α-Synuclein fibrils using any one of the antibodies of the disclosure.

Dysglycemia as a risk factor for neurodevelopmental disorder or developmental diabetes. The risk is assessed based on measurement of a glucose control indicator in a blood sample. One particular example of a neurodevelopmental disorder is retinopathy of prematurity in an infant. One particular example of a glucose control indicator is ‘comprehensive glycated hemoglobin fraction’ or ‘comprehensive glycated albumin fraction.’ This is calculated using ‘total whole blood protein’ in the denominator. In the case of chronic hyperglycemia, there is an increased risk of proliferative retinopathy of prematurity. In the case of chronic hypoglycemia, there is an increased risk of non-proliferative retinopathy of prematurity. This ‘total whole blood protein’ technique could also be used to determine the glucose control status in other types of patients.