The present disclosure provides for the diagnosis and prediction of neuromyelitis optica (NMO) in subject. It also provides for treatment of multiple sclerosis (MS) in a subject. Thus, in accordance with the present disclosure, there is provided a method for treating a subject having neuromyelitis optica (NMO) comprising administering to said subject an inhibitor of B-cell activating factor (BAFF) and/or an inhibitor or proliferating inducing ligand (APRIL).

Provided herein are Amyotrophic lateral sclerosis (ALS) biomarkers and methods of using these ALS biomarkers to diagnose and treat ALS.

Processes and materials are provided for the detection, diagnosis, or determination of the severity of a neurological injury or condition, including traumatic brain injury, multiple-organ injury, stroke, Alzeimer's disease, Parkinson disease and Chronic Traumatic Encephalopathy (CTE). The processes and materials include biomarkers detected or measured in a biological sample such as whole blood, serum, plasma, or CSF. Such biomarkers include Tau and GFAP proteins, their proteolytic breakdown products, brain specific or enriched micro-RNA, and brain specific or enriched protein directed autoantibodies. The processes and materials are operable to detect the presence of absence of acute, subacute or chronic brain injuries and predict outcome for the brain injury.

Life-threatening traumas such as terrorist attacks, war, disasters, mental or physical assault, severe accidents and violence frequently provoke emotional and behavioral disturbances known as post-traumatic stress disorder (PTSD) and suicide related thereto. Accurate diagnosis and treatment planning for PTSD and suicide remain difficult. The discovery of specific markers creates new opportunities for more accurate clinical assessments identifying groups that may experience better outcomes when exposed to an intervention. The present invention provides a process of detection of P-11, UBE3A, STY1, EMAP-II, SIP1, ORC5L, DCX, SCYE protein in a biological sample of a subject suspected of suffering from PTSD and/or having suicidal tendencies, and provides additional PTSD markers which are specific to gender.

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

In one aspect, the invention provides a method for alleviating a symptom in a patient with amyotrophic lateral sclerosis, comprising administering an efficacious therapeutic that is efficacious to the patient, the efficacious therapeutic, when administered to the patient, resulting in a level of a neurofilament protein in a biological sample of the patient that is lower than a level of neurofilament protein in a patient with amyotrophic lateral sclerosis not administered the therapeutic. In some embodiments, the patient is currently being administered with or has formerly been administered with either a non-efficacious therapeutic or a therapeutic that is different than the efficacious therapeutic.

A method involves detecting in a sample an autoantibody binding specifically to a mammalian VGLUT. An autoantibody binding specifically to a mammalian VGLUT and a diagnostically useful carrier with a solid phase with an immobilized polypeptide containing a mammalian VGLUT or a variant thereof, are useful. The autoantibody can be used for diagnosing a neurological autoimmune disease or a cancer.

The present invention provides, inter alia, methods for identifying a candidate agent that may be effective to treat or ameliorate an effect of a neurodegenerative disease in a subject. These methods include: (a) contacting a wildtype neuron and a mutant neuron with a stressor which is effective to accelerate the degeneration of the mutant neuron; (b) further contacting the wildtype neuron and the mutant neuron from step (a) with a candidate agent; and (c) determining whether the candidate agent lowers a wildtype to mutant survival ratio or increases both wildtype and mutant neuron survival.

The present invention relates to anti-alpha-synuclein (anti-α-synuclein) antibodies and methods of using the same.

Provided are novel human copper-zinc superoxide dismutase, also known as superoxide dismutase 1 or SOD1, specific antibodies as well as fragments, derivatives and variants thereof as well as methods related thereto. Assays, kits, and solid supports related to antibodies specific for SOD1 are also disclosed. The antibody, immunoglobulin chain(s), as well as binding fragments, derivatives and variants thereof can be used in pharmaceutical and diagnostic compositions for SOD1 targeted immunotherapy and diagnosis, respectively.