Abstract: This invention relates to methods for improved cell-based therapies for retinal degeneration and for differentiating human embryonic stem cells and human embryo-derived into retinal pigment epithelium (RPE) cells and other retinal progenitor cells.

Abstract: The present invention relates to a composition for regulating circadian rhythms, a composition for diagnosing circadian rhythm disorders and a diagnostic kit, wherein the composition for regulating circadian rhythms comprises NQ peptides, C12orf39 genes, NQ peptides cDNA and the like, which relate to circadian regulation in vertebrates as main components.

Abstract: The present invention relates to modified eIF4G1 peptides, uses thereof and pharmaceutical compositions comprising the modified eIF4G1 peptides.

Abstract: The invention describes antibodies having a high affinity for aggregated forms of ?-synuclein and a low affinity for monomeric forms of ?-synuclein. The antibodies are useful in the diagnosis of neurodegenerative diseases.

Abstract: The invention provides a method for preparing a peptide for improving brain function, comprising hydrolyzing milk casein with an enzymatic catalyst comprising a protease to produce a hydrolysate comprising: (i) a peptide consisting of the amino acid sequence shown in SEQ ID NO: 1 or a variant thereof; (ii) a peptide consisting of the amino acid sequence shown in SEQ ID NO: 2 or a variant thereof; or (iii) a mixture of the peptides of (i) and (ii), wherein the production yield of each of the peptides is 2% or more, or the total production yield of the mixture is 10% or more. The invention also provides a food or drink or a pharmaceutical composition containing the hydrolysate.

Abstract: A method for diagnosing the presence of hereditary spastic paraplegia (HSP) or predicting the risk of developing HSP in a human subject, comprising detecting the presence or absence of a defect in a gene encoding a polypeptide comprising the sequence of FIG. 9 (SEQ ID NO: 19), in a nucleic acid sample of the subject, whereby the detection of the defect is indicative that the subject has or is at risk of developing HSP.

Abstract: An assay for Alzheimer's disease pathology (AD) in a living patient is disclosed wherein an amount of ?7nAChR-FLNA, TLR4-FLNA and/or ?7nAChR-A?42 complex present as a protein-protein complex in a sample is determined and compared to the amount in a standard sample from a person free of AD pathology. Use of one or more of those ratios provides an assay predictive of prognosis for treatment with a medicament in which the amount of an above protein complex is determined and compared to an amount determined in the presence of a medicament that binds to a FLNA pentapeptide and contains at least four of the six pharmacophores of FIGS. 7-12. An amount of protein complex determined in the presence of the medicament less than the first determined amount indicates a favorable treatment prognosis.

Abstract: The present invention relates to development, validation and application of new sets of biomarkers for diagnosis of Alzheimer's disease (AD) and related disorders including early diagnosis of MCI and early prodrome of AD, identification of disease sub types, prediction of their response to disease management procedures, drugs and their combinations and for monitoring response for these treatments, including validation of biomarkers for clinical trials.

Abstract: The present invention provides methods for diagnosing mental disorders. The invention also provides methods of identifying modulators of mental disorders as well as methods of using these modulators to treat patients suffering from mental disorders.

Abstract: The present invention provides methods of treating epilepsy and other neurological disorders. The methods generally involve administering to an individual in need thereof an effective amount of an agent that blocks a transforming growth factor-beta pathway.

Abstract: This document provides methods and materials for detecting C9ORF72 hexanucleotide (GGGGCC) (SEQ ID NO: 3) repeat expansion positive (C9+) frontotemporal lobar degeneration or C9+ amyotrophic lateral sclerosis. For example, methods and materials related to using anti-(GP)8 (SEQ ID NO: 2) antibodies to identify mammals (e.g., humans) having C9+ FTLD or C9+ ALS are provided.

Abstract: The present invention relates to an antibody which specifically binds to unprocessed and/or partially processed neurotoxin polypeptide or an antibody which specifically binds an epitope consisting of a peptide having an amino acid sequence as shown in any one of SEQ ID NOs: 1 to 16 and to methods for the manufacture of such antibodies. Moreover, the present invention relates to a composition comprising processed neurotoxin polypeptide free of unprocessed or partially processed neurotoxin polypeptide and a method for manufacturing said neurotoxin polypeptide based on the antibodies of the invention. The present invention also relates to the use of the aforementioned antibody for separating processed neurotoxin polypeptides from unprocessed or partially processed neurotoxin polypeptides or for determining unprocessed or partially processed neurotoxin polypeptides. The present invention relates to a method for the manufacture of a medicament.

Abstract: Disclosed herein are methods for treating amyloid disease in humans by clearing amyloid peptides from one or more bodily fluids such as, e.g., blood, of a patient. In particular, the methods are based on the administration of compounds capable of binding to amyloid-beta (A?) or on dialysis of blood or plasma exchange in order to remove A? peptides from the blood circulation, and/or brain or other affected organs.

Abstract: It has been discovered that that certain growth factors can delay the ossification of a tissue site, such as a cranial suture, via the promotion of fibroblast differentiation and/or inhibition of osteoblast differentiation. Provided herein are methods for treating bone formation conditions or disorders, such as synostotic conditions, or ectopic mineralization conditions, via administration of compositions comprising connective tissue growth factor (CTGF), and optionally other growth factors or fibroblast or progenitor cells, to a tissue site of a subject in need thereof.

Abstract: The present invention provides novel therapeutics and methods of treatment for diseases associated with activation of the advanced glycatio? endproducts receptor (RAGE).

Abstract: Compositions comprising monoclonal antibodies raised against CAP37 (Cationic Antimicrobial Protein of Mr 37 kDa) and isoforms thereof, along with antigen binding fragments thereof, are disclosed. The antibodies are used in the diagnosis and early detection of Alzheimer's disease and Age-Related Macular Degeneration.

Abstract: The present application relates to isolated proteins, particularly monoclonal antibodies, in particular CDR-grafted, humanized antibodies which bind to RAGE protein. Specifically, these antibodies have the ability to inhibit the binding of RAGE to its various ligands. The antibodies or portions thereof of described in the present application are useful for treating a disease or disorder characterized by or induced by pathophysiological ligands of RAGE, for example missfolded proteins like amyloid ? and advanced glycation-end-products.

Abstract: The present invention relates to polypeptides derived from single domain heavy chain antibodies directed to Tumor Necrosis Factor-alpha. It further relates to single domain antibodies that are Camelidae VHHs. It further relates to methods of administering said polypeptides. It further relates to protocols for screening for agents that modulate the TNF-alpha receptor, and the agents resulting from said screening.

Abstract: The present invention is directed to a method for treating an inflammatory neurodegenerative condition of the CNS in a subject comprising administering to said subject a G-CSF or G-CSFR inhibiting agent selected from the group consisting of an antibody specific for G-CSF or G-CSFR, a soluble G-CSFR or a G-CSF-binding portion thereof and a 20 to 30 nucleotide sense or antisense molecule targeted to a nucleic acid molecule encoding G-CSF.

Abstract: The present invention is directed to a method for treating an inflammatory neurodegenerative condition of the CNS in a subject comprising administering to said subject a G-CSF or G-CSFR inhibiting agent selected from the group consisting of an antibody specific for G-CSF, a soluble G-CSFR or a G-CSF-binding portion thereof and a 20 to 30 nucleotide sense or antisense molecule targeted to a nucleic acid molecule encoding G-CSF.