The present disclosure provides a method of increasing the functionality of a GABAergic interneuron in the hilus of the hippocampus of an individual having at least one apolipoprotein E4 (apoE4) allele. The method generally involves reducing tau levels in the interneuron.

Peptide analogues of ?-amyloid and methods of using said analogues for neuroprotection are described herein. The ?-amyloid peptide analogues have a sequence that is at least 50% identical to an N-terminal ?-amyloid core fragment. A pharmaceutical composition of the ?-amyloid peptide analogues in a pharmaceutically acceptable carrier can be administered to a subject for neuromodulation. The ?-amyloid peptide analogues, while lacking neurotoxicity, effectively provides for protective activity against ?-amyloid toxicity.

The invention relates to a compound for use for inducing apoptosis in a cancerous cell, wherein said compound is selected from the group consisting of ApoO, a variant or a fragment thereof, their mixtures, and a vector encoding for said ApoO, variant or fragment thereof. The invention further relates to a compound for use for treating a pathophysiological situation, wherein said compound is an inhibitor of the ApoO activity or of the ApoO gene expression.

The invention relates to antibodies, antibody fragments and binding agents that specifically recognizes oligomeric A that is resistant to denaturation by SDS but does not bind monomeric, fibrillar or other oligomeric forms of A that are generated in vitro.

Disclosed herein are compositions and methods for treating and preventing neurodegenerative diseases, such as Alzheimer's disease. In some embodiments, the composition comprises a peptide that disrupts the binding between PTP and APP, preventing -amyloidogenic processing of APP without affecting other major substrates of - and -secretases. Alternatively, in some embodiments, an antibody or a fragment of an antibody against PTP or APP may be used to disrupt the binding between PTP and APP. In some embodiments, the composition comprises compounds or enzymes, which restore perineuronal balance of PTP ligands CS and HS, thereby preventing abnormally increased -amyloidogenic processing of APP. Compositions and methods disclosed herein can be used in combination to treat and prevent neurodegenerative diseases.

A pharmaceutically acceptable aqueous gel composition comprising a gelling agent, magnesium and/or manganese, or bivalent ions thereof, and an mRNA molecule encoding a protein of interest; and methods for inducing or facilitating repair, re-generation or generation of tissue in a human or animal subject, comprising administering the composition to the site of the tissue to be repaired, re-generated or generated.

The present disclosure provides methods for identifying a human subject at risk of developing progressive renal decline by examining a level(s) of a protective protein(s) in a sample from the subject. Level(s) of protein(s) identified in the disclosure are associated with protection against progressive renal failure and end-stage kidney disease (ESKD). Examples of such protective proteins include FGF20, ANGPT1, and TNFSF12.

A non-invasive CEST MRI imaging method is disclosed for early detection and mapping the severity of diseases by using MRI. The endogenous magnetic resonance image (MRI) contrast of the biological tissue can rely on the endogenous protons of the proteins and peptides as a source of the contrast, such as hydroxyl, amine, and amide protons, and thereby provide imaging of the accumulation of amyloid beta, accumulation of neurofibrillary tangles, aggregation proteins and peptides, the hypoxia in cancer and non-cancer tissue, the tissues atrophy, distinguish the edema from the tumor, determine tumor boundary, monitor response of tumor to treatment and detect lower grade tumor by using endogenous protons contrast via CEST MRI. The difference in CEST images signals is used to detect and map severity of the diseases and predict response to treatment. The method works without contrast agents or tracers.

The invention relates to a compound for use for inducing apoptosis in a cancerous cell, wherein said compound is selected from the group consisting of ApoO, a variant or a fragment thereof, their mixtures, and a vector encoding for said ApoO, variant or fragment thereof. The invention further relates to a compound for use for treating a pathophysiological situation, wherein said compound is an inhibitor of the ApoO activity or of the ApoO gene expression.

Disclosed are methods and compositions for targeting antibodies to amyloid deposits. For example, amyloid-reactive peptides that bind amyloid deposits are administered to a subject. Antibodies to the amyloid-reactive peptides are then administered to the subject. Upon administration of the antibodies, the amyloid-reactive peptides bind the antibodies and thus pre-target the antibodies to the amyloid deposits. In other examples, an amyloid-reactive fusion peptide contains an epitope of a known antibody. When the fusion peptide is administered to a subject, the fusion peptide binds amyloids in the subject. Administration to the subject of the known antibody that binds the epitope of the fusion peptide then targets the antibody to the amyloid deposit to which the fusion peptide is bound.