The present disclosure provides methods of treating inflammatory indications with complement inhibitor compounds and compositions. Included are compounds and methods for treating amyotrophic lateral sclerosis (ALS).

The present invention relates to the field of medicine and in particular to Parkinson's disease (PD). Specifically the present invention relates to methods and means for early detection of PD. The invention relates also to methods and means for treatment or prophylaxis of PD. In the method of the invention a probability of a subject developing or having Parkinson's disease (PD) is determined by measuring the relative abundances of one or multiple microbial taxa in a sample from a subject; and the probability of the subject developing or having PD is determined based on the measured abundances. The present invention provides a novel approach for the diagnostics of PD.

The invention relates to methods of identifying compounds that modulate mTORC1 activity in a cell by modulating the activity of SAMTOR, as well as to the use of such identified compounds in the modulation of mTORC1 and the treatment of diseases and conditions characterized by aberrant mTORC1 activity.

The invention provides anti-Tau antibodies and methods of using the same.

Methods and materials herein are useful for assessing and/or treating autoimmune ataxias associated with septin-specific autoantibodies septin-5-specific autoantibodies For example, septin-5 polypeptides are provided as well as methods for using septin-5 polypeptides to detect septin-5-specific autoantibodies and/or to treat a mammal having an autoimmune ataxia.

Methods and materials herein are useful for assessing and/or treating autoimmune ataxias associated with septin-specific autoantibodies (e.g., septin-5-specific autoantibodies). For example, septin-5 polypeptides are provided as well as methods for using septin-5 polypeptides to detect septin-5-specific autoantibodies and/or to treat a mammal having an autoimmune ataxia.

Provided herein are compositions and methods for reducing toxicity associated with TAR DNA-binding protein 43. Certain embodiments of the present disclosure are related to compositions that treat, inhibit, reduce, prevent, or delay a disease or condition associated with TDP-43 toxicity, such as cystic fibrosis or neurodegenerative diseases. Certain embodiments of the present disclosure are related to methods of treating, inhibiting, reducing, preventing, or delaying a disease or condition associated with TDP-43 toxicity by administering compounds of any one of Formulas (I), (II), (III), (IV), (V), (VI), (VII), or (VIII) to a subject in need.

The present invention relates to binding agents of human Leucine-rich Repeat Kinase 2 (LRRK2). More particular, allosteric modulators of LRRK2 activity have been identified, for targeting LRRK2 in human cells, while leaving LRRK2 subcellular localisation unaffected. Even more specifically, protein binding agents for allosteric modulation of LRRK2 kinase activity are disclosed, comprising immunoglobulin single variable domains (ISVDs) binding to human LRRK2 with nanomolar affinity. The invention thus reveals means and methods for a novel LRRK2 targeting approach through allosteric modulation of its activity for use in treatment of LRRK2-related pathologies, such as Parkinson's disease, as well as for use in detection of LRRK2 in vitro and in vivo, and for use as a diagnostic.

An assay is disclosed based on the successful transmission of DLB, and to a much lesser extent PD, to cultured HEK cells expressing the A53T and E46K point mutation. DLB prion activity was achieved by treatment of brain homogenates with detergent extraction and limited proteolysis followed by polyoxometalate precipitation of the prions. The results show the MSA strain of α-synuclein prions differs from those causing PD and DLB. Manipulating dominant negative inhibition of α-synuclein prions has created a new approach to identifying novel prions and deciphering the features of their multiplication.

Embodiments of the disclosure include treatments of subconcussive and/or concussive brain damage by administering fibroblasts and/or fibroblasts cultured with one or more types of immunocytes. In one specific embodiment fibroblasts are cultured with monocytes in the presence of patient-specific T cells, and subsequently the T cells are re-administered into the patient. In one particular embodiment, products derived from fibroblast-immunocyte mixtures are comprised of cellular lysate, apoptotic bodies, exosomes, and/or other microvesicles. In one embodiment, the fibroblast cells and/or products derived from the fibroblast cells are administered subsequent to one or multiple head injuries. In other embodiments, products are administered in combination with neurorestorative and/or neuroprotective interventions.