In one aspect, methods of diagnosing a subject as having Alzheimer's disease and prognosing a subject as being at risk of progressing to Alzheimer's disease are provided. In some embodiments, the method comprises determining one or more of the level of expression of rhotekin 2 (RTKN2), the level of expression of microtubule-associated Ser/Thr kinase 4 (MAST4), the level of binding of forkhead box O1 (FOXO1) to the RTKN2 promoter, and the level of binding of amyloid precursor protein (APP) to the MAST4 promoter in a sample from the subject.

A method and a system are provided for taking biomarker measurements of patients who have ADHD. Mathematical analysis (e.g., pattern recognition, machine learning and AI algorithms) of the biomarker measurements is used to create a unique personal prediction model and data set for an individual patient. The unique personal data set is used to diagnose and monitor a particular problem of the individual patient associated with ADHD, or to recommend a treatment for a particular problem of the individual patient associated with ADHD, or to predict an outcome of a treatment for a particular problem of the individual patient associated with ADHD.

Provided is a method for diagnosing a subject having or at risk of having mild cognitive impairment (MCI), including stimulating T cells in a biological sample obtained from the subject with an amyloid β peptide or a fragment thereof and evaluating a magnitude of a T cell response toward the amyloid β peptide or the fragment thereof. Also provided is a kit for diagnosing MCI by using the method.

The invention provides methods of detecting alpha-synuclein using a capture antibody and a reporter antibody. The capture antibody binds preferentially to full-length alpha-synuclein phosphorylated at residue 129 (PS129 alpha-synuclein) over unphosphorylated full-length alpha-synuclein. The 11A5 antibody is an example of a suitable capture antibody. The reporter antibody binds to an epitope within residues 40-55 of alpha-synuclein. The 23E8 antibody is an example of such an antibody. Because only a small proportion of alpha-synuclein is phosphorylated high sensitivity of detection below picomolar is advantageous.

The disclosure discloses anti α-Syn antibodies preferentially recognizing α-Syn aggregates. The antibodies of the present invention bind to α-Syn aggregates with high affinity and specificity and inhibit accumulation or intercellular transfer of α-Syn aggregates, and thus can be used for detection, diagnosis and/or treatment or prevention of various diseases caused by the accumulation of α-Syn aggregates.

A method for identifying pre-disposition to cognitive decline in a subject, the method comprising determining levels of: (a) omega-3 fatty acids, and vitamin D or a metabolite thereof; (b) omega-3 fatty acids, and homocysteine; (c) vitamin D or a metabolite thereof, and homocysteine; or (d) omega-3 fatty acids, vitamin D or a metabolite thereof, and homocysteine, independently in one or more samples obtained from the subject.

The invention relates to methods for selective quantification of A-beta or alpha-synuclein aggregates comprising the immobiliZation of anti-A-beta or alpha-synuclein antibodies on a substrate, application of the stool sample to be tested to the substrate, addition of probes labelled for detection which by specific binding to A-beta or alpha-synuclein aggregates mark these and detection of the marked aggregates.

The invention provides antibodies that specifically bind human α-synuclein with a high affinity and reduces α-synuclein spreading in vivo, recombinant polypeptides comprising said antibodies or antigen-binding fragment thereof and methods for generating such polypeptides, as well as compositions and methods for generating α-synuclein antibodies, and methods of using α-synuclein antibodies for the treatment of diseases of the central nervous system, in particular alpha-synucleinopathies.

The present invention relates to a composition for preventing or treating Alzheimer’s disease, containing an inhibitor of ATL2, and a method of diagnosing the disease based on the measurement of the ATL2. In the present invention, it was found that PS1 mutants may result in mitochondrial dysfunction, such as increased binding between endoplasmic reticulum and mitochondria, increased mitochondrial ROS production, decreased mitochondrial membrane potential, decreased ATP production, decreased complex I activity, and decreased peroxidase activity, in brain glioma cells and that the PS1 mutants may abnormally increase the binding between endoplasmic reticulum and mitochondria by elevating the expression of the ATL2 in the brain. In addition, when the ATL2 was knocked down, it was observed that the binding between endoplasmic reticulum and mitochondria was lowered and that the expression of the ATL2 was elevated in the brains of Alzheimer’s disease animal models and patients. Accordingly, it is expected that it may possible to effectively prevent or treat Alzheimer’s disease by inhibiting the expression or activity of the ATL2 and that it may possible to diagnose the disease, predict the risk of developing the disease, and screen therapeutic agents for the disease, by measuring the level of the expression or activity of the ATL2.

The present invention can be included in the field of medicine. Specifically, the present invention provides antibodies and antigen-binding fragments thereof which can bind isoAsp7 amyloid β (Aβ) and a pharmaceutical composition comprising the antibodies or antigen-binding fragments thereof. IsoAsp7 Aβ can be found in plaques of Alzheimer's patients and is thus a suitable target for the treatment and/or prevention of Aβ-related diseases such as Alzheimer's disease. Thus, the antibodies, antigen-binding fragments thereof and the pharmaceutical composition comprising either can be used to treat and/or prevent neurodegenerative diseases. Further, the present invention provides hybridoma cell lines, the use of the antibodies or antigen-binding fragments thereof for the diagnosis and/or prognosis of a neurodegenerative disease and a method for detecting isoAsp7 Aβ in an isolated sample.