The present disclosure provides methods for the treatment of a mammal having a neurological condition, disease, or injury. The methods involve increasing the number of functional GABAergic interneurons at or near the site of the neurological disease, injury, or condition.

Described herein are methods and systems for the detection of anti-vinculin antibodies, for determining a presence or likely presence of a gastrointestinal motility disorder, bladder motility disorder, or fibromyalgia. Further provided are methods of selecting and/or administering a therapy based on the presence or absence of anti-vinculin antibodies.

Diagnostic methods are useful for diagnosing neuropathic pain in a subject, for predicting whether a subject is at risk of developing neuropathic pain, or for determining whether a neuropathic pain therapy is successful. Tools for carrying out the aforementioned methods, include diagnostic devices, and oxidized lipids, for example, an epoxylipid, for use in the aforementioned methods.

The invention generally relates to optical methods for the diagnosis of neuronal condition by converting a cell from a patient into a neuron and optically evaluating action potentials of that cell in vitro. The cell is transformed with an optical reporter and exhibits an optical signature in response to neural stimulation. Using genome-editing, a control cell can be made that is isogenic butfor a known mutation and a control signature obtained from the control cell. Thus, methods of the invention reveal potential neurodegenerative effects of a mutation as manifested in a patient's genetic context. The optical signature of the cell, or the difference between the signature and the control signature, is correlated to a diagnosis of the neurodegenerative disease

The present invention relates to a new p75NTR neurotrophin binding protein (NBP)-Fc fusion protein comprising a p75NTR (NBP) portion and an immunoglobulin portion. In certain embodiments, the p75NTR (NBP)-Fc fusion protein is for use in the treatment of pain and/or a symptom of pain.

The present invention achieves a therapy and/or exercise instructing process management that is capable of providing an exercise menu sufficiently suited for an exerciser by considering the state of the body of the exerciser. The above object is achieved to provide a therapy and/or exercise instructing process management system implemented by a client-side terminal operated by a client and a trainer-side terminal that is connectable to the client-side terminal via communication and operated by a trainer, the system including: an assessor that assesses a posture of the client in a steady state and/or a moving state; an exercise determiner that determines exercise to be performed by the client based on an assessment made by the assessor; and a storage that stores information regarding the assessment made by the assessor and information regarding the exercise that is determined by the exercise determiner and performed by the client.

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.

The invention generally relates to optical methods for the diagnosis of neuronal condition by converting a cell from a patient into a neuron and optically evaluating action potentials of that cell in vitro. The cell is transformed with an optical reporter and exhibits an optical signature in response to neural stimulation. Using genome-editing, a control cell can be made that is isogenic but-for a known mutation and a control signature obtained from the control cell. Thus, methods of the invention reveal potential neurodegenerative effects of a mutation as manifested in a patient's genetic context. The optical signature of the cell, or the difference between the signature and the control signature, is correlated to a diagnosis of the neurodegenerative disease.

The disclosure relates to methods for pain management in the perioperative context, particularly through the use of the DNA methylation status of the human OPRM1 gene as a biomarker for increased susceptibility to perioperative pain, and related methods and compositions.

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.