Abstract: The invention belongs to the fields of diagnostic, prognostic, and monitoring assays of neurological disorders involving Tau dysfunction. A direct interaction between proteins FKBP52 and Tau is reported. Herein are described methods for testing a subject thought to have or be predisposed to having a neurological disorder involving Tau dysfunction; and also for preventing or treating a neurological disorder involving Tau dysfunction in a subject in need thereof.

Abstract: The present technology generally is directed to methods for treating mild brain injury and other neurological disorders in a subject. The methods can include administering to the subject an effective amount of a compound comprising ghrelin. The present technology is also generally directed to methods for treating mild brain injury and other neurological disorders in a subject, for example, by administering to the subject an effective amount of a compound comprising ghrelin modified to include octanoic acid or by limiting the carbon 14 content.

Abstract: The present invention relates to compositions and methods for neuroprotection. In particular, provided herein are compositions (e.g., hepatocyte secretory factors) for alleviating and/or protecting against neuronal damage (e.g., resulting from stroke), and methods of use thereof.

Abstract: The present invention is directed to methods of preventing central nervous system leukemia, treating T-cell acute lymphoblastic leukemia, and treating immune system disorders associated with CCR7-CCL19 mediated signaling. Suitable therapeutic agents for inhibiting CCR7-CCL19 signaling and methods of identifying additional therapeutic agents useful in the methods of the present invention are also disclosed.

Abstract: The invention relates generally to treatment of neurological disorders and nervous system injuries. The invention specifically provides methods of using modulators of particular target proteins to modulate degeneration of neurons or portions thereof, such as axons.

Abstract: Described herein are compositions and methods for enhancing peripheral macrophage A? phagocytosis activity. The methods include inhibiting the TGF-? signaling pathway and activating the BMP signaling pathway in peripheral macrophages to promote central nervous system infiltration and enhance macrophage A? phagocytosis activity. Inhibition of TGF-? signaling and activation of BMP signaling in peripheral macrophages represents an advantageous anti-amyloid therapeutic approach for Alzheimer's disease.

Abstract: Agents that reduce the level of a tau gene product in a cell, e.g., in a neuron, include antisense nucleic acids. For example, antisense nucleic acids can be used to down-regulate expression of a tau gene in a cell (e.g., in a neuron). The antisense sequence is complementary to the mRNA of the targeted gene (e.g., tau), and inhibits expression of the targeted gene products. Suitable oligonucleotides can be chemically modified from the native phosphodiester structure, in order to increase their intracellular stability and binding affinity. A number of such modifications have been described in the literature, which modifications alter the chemistry of the backbone, sugars, or heterocyclic bases.

Abstract: In an in vivo method for detecting ?-synuclein protofibrils in human tissue, an antibody or fragment thereof is administered to a human. The antibody or fragment is labelled with a detectable label. A complex formed between the antibody or fragment and ?-synuclein protofibrils in the human tissue is detected. The antibody or fragment has high affinity for human ?-synuclein protofibrils and low affinity for ?-synuclein monomers and has a combination of three specified variable heavy (VH) CDR sequences and three specified variable light (VL) CDR sequences.

Abstract: The present invention provides the use of the cell surface antigen CD51 as a negative selection marker for neuronal cells and a method for enrichment, isolation and/or detection of neuronal cells comprising the steps a) contacting a sample containing neuronal cells with an antigen-binding fragment specific for the CD51 antigen coupled to a solid phase, thereby labeling the CD51 positive cells of said sample and b) isolating the non-labeled cells of said sample.

Abstract: The invention is based in part on identifying a core region of ND2 responsible for interacting with Src to within residues 289-321 of ND2 and more particularly residues 307-321 or 310-321 of ND2. Peptides including, overlapping or from within this region can be used to inhibit ND2 interaction with Src Inhibition of this interaction is useful for treatment or prophylaxis of neurological diseases and disorders, pain and cancer.

Abstract: The present disclosure provides methods of treating a tauopathy, involving administering an anti-Tau antibody. The present disclosure also provides anti-Tau antibodies, and formulations comprising same, for use in the methods.

Abstract: A pharmaceutical formulation and method of treatment of prion disease include a RAP agent with a pharmaceutically acceptable carrier and/or excipient, and the administration of same to a subject suffering from or at risk of a prion disease. The RAP agent is an effective means for the prevention and/or treatment of various prion diseases regardless whether the disease is acquired by infection or by genetic mutation.

Abstract: Methods, agents and devices for treating a patient to reduce accumulation of certain proteins in the brain are described. Such proteins include A?, and the methods, agents and devices are useful for reducing the accumulation of A?, which is a principal constituent of the plaques associated with such diseases as Alzheimer's disease (AD). Antibodies to A?, when delivered systemically or directly into the central nervous system, improve cognitive deficits in a transgenic mouse model of AD. However, unlike peripheral of antibodies to A?, which increased cerebral vascular plaques and hemorrhages, direct central administration did not result in such an increase cerebral vascular plaques and hemorrhages.

Abstract: The invention relates to an isolated antibody, or fragment thereof, having high affinity for human A? protofibrils. The invention further relates to compositions that include the antibody, or a fragment thereof, and a pharmaceutically acceptable buffer. The invention further relates to a method of preventing or treating Alzheimer's disease, which includes the step of administering to a patient having or suspected of having Alzheimer's disease such an antibody, or fragment thereof or a composition that includes the antibody or a fragment thereof.

Abstract: A method for detecting the risk of Alzheimer's disease comprises detecting immunomagnetic reduction signals of two biological markers in a biological sample from a subject, wherein the two biological markers are tau protein and A?-42 protein; and calculating concentrations of the above two biological markers and using the product of the concentrations of the above two biological markers to diagnose the risk of Alzheimer's disease, wherein the concentration is calculated by the conversion of the magnetic reduction signals.

Abstract: In one aspect, the invention relates to a method for identifying a drug candidate with activity as a neuroprotective agent. The method includes determining whether a compound reduces ATF4 activity; and identifying the compound that reduces ATF4 activity as a drug candidate.

Abstract: Fusion proteins that contain the fusion of (i) a peptide of less than 100 amino acids comprising a first amino acid sequence comprising AASSG (SEQ ID NO: 1) and a second amino acid sequence comprising XAGXDXXTEXPXS (SEQ ID NO: 2), wherein X designates any amino acid, and (ii) a protein transduction domain (PTD) are provided, along with pharmaceutical compositions containing the fusion protein. The proteins can be used to treat Huntington's disease.

Abstract: The present disclosure provides methods of treating a tauopathy, involving administering an anti-Tau antibody. The present disclosure also provides anti-Tau antibodies, and formulations comprising same, for use in the methods.

Abstract: The present disclosure provides methods of treating a tauopathy, involving administering an anti-Tau antibody. The present disclosure also provides anti-Tau antibodies, and formulations comprising same, for use in the methods.

Abstract: Antibodies and fragments thereof have high affinity for human ?-synuclein protofibrils and low binding of ?-synuclein monomers, wherein the antibodies or fragments have specified Complementarity Determining Region (CDR) sequences. Compositions comprise such an antibody or fragment and methods of detecting ?-synuclein protofibrils use such an antibody or fragment. In further embodiments, methods of preventing, delaying onset of or treating a neurodegenerative disorder with ?-synuclein pathology comprise administering such an antibody or fragment, and such an antibody or fragment is used in the manufacture of a pharmaceutical composition for treatment of a neurodegenerative disorder with ?-synuclein pathology. Such an antibody or fragment is used in the diagnosis or monitoring of the development of a neurodegenerative disorder with ?-synuclein pathology, and in methods for reducing or inhibiting ?-synuclein aggregation by administration of such an antibody or fragment.