The present disclosure provides methods and compositions for the treatment of diseases and genetic disorders linked to SLC6A1 loss and/or misfunction. The methods and compositions of the present disclosure comprise rAAV vectors and rAAV viral vectors comprising transgene nucleic acid molecules comprising nucleic acid sequences encoding for a GAT1 polypeptide.

Provided herein are fusion constructs including a biologically active agent such as an antibody or derivative thereof which is functionally linked with a functional moiety such as an LC3 protein or portion thereof. Also provided are compositions and exosomes including such constructs, as well as methods for preparing exosomes containing such constructs, and methods for delivering such constructs to cells. Methods and uses of such constructs and exosomes for treating diseases or disorders are also provided, in which the constructs trigger autophagy of disease-related cellular or cytoplasmic targets such as misfolded/aggregated proteins in neurodegenerative diseases, for example.

The invention provides a combination treatment for ischemia conditions in or otherwise affecting the CNS, such as stroke. The treatment invoices administration of a PSD-95 inhibitor and performing reperfusion therapy (e.g. by administration of tPA). Administration a PSD-95 inhibitor in combination with reperfusion therapy increases the efficacy of the reperfusion therapy and/or slows the decline in efficacy of reperfusion therapy with time after onset of ischemia thus extending the window in which reperfusion therapy can be administered.

The invention provides a combination treatment for ischemia conditions in or otherwise affecting the CNS, such as stroke. The treatment invoices administration of a PSD-95 inhibitor and performing reperfusion therapy (e.g. by administration of tPA). Administration a PSD-95 inhibitor in combination with reperfusion therapy increases the efficacy of the reperfusion therapy and/or slows the decline in efficacy of reperfusion therapy with time after onset of ischemia thus extending the window in which reperfusion therapy can be administered.

The invention relates to a supramolecular aggregate of formula (VI) wherein A is an active substance, and X.sub.1, X.sub.2, X.sub.3 and X.sub.4, independently to each other, are a moiety of Formula (I) containing a maleimido functionalization and at least one among X.sub.1, X.sub.2, X.sub.3 and X.sub.4 is present in Formula (VI). In a preferred embodiment the maleimido-functionalized core is PWT2. The supra-molecular aggregate can be used in the field of drugs, vaccines, as ligands for GPCR, i.e. agonists as well as antagonist, as antibiotics and as diagnostics eventually in complex with radionuclides.

The present invention relates to anti-depression and anti-anxiety application of a polypeptide, and provides application of a polypeptide having a sequence as shown in SEQ ID NO: 1 in preparation of a medicine for treating and/or preventing depression or anxiety. The present invention further relates to a complex containing the polypeptide.

The present disclosure provides methods and compositions for the treatment of diseases and genetic disorders linked to SLC6A1 loss and/or misfunction. The methods and compositions of the present disclosure comprise rAAV vectors and rAAV viral vectors comprising transgene nucleic acid molecules comprising nucleic acid sequences encoding for a GAT1 polypeptide.

The present disclosure provides compositions, methods, and kits that enable the in situ growth of polymers on or within a subject. In some aspects, the monomer, dopamine, polymerizes in vivo to form a polymer on a tissue. In additional aspects, the compositions, methods, and kits are useful for treating or preventing a disease or disorder.

The invention provides a therapeutically-effective method for treatment of heart failure (HF), chronic heart failure, and heart failure post myocardial infarction (MI). This method treats heart failure by enhancing cardiac contractility in a patient by activating -arrestin 2 to enhance sarco(endo) plasmic reticulum Ca.sup.2 ATPase (SERCA-2a) small ubiquitin-like modifier-ylation (SUMOlation). Thus, -arrestin 2 stimulates cardiac function in heart failure via SERCA-2a potentiation. Additionally, the invention provides a composition for increasing cardiac contractility including a -1 adrenergic receptor (-1 AR) ligand that induces -arrestin 2 binding to a -1 adrenergic receptor.

The present invention relates to combinations comprising a positive allosteric modulator (PAM) of metabotropic glutamatergic receptor subtype 2 (mGluR2) or a pharmaceutically acceptable salt or a solvate thereof, or an orthosteric agonist of metabotropic glutamatergic receptor subtype 2 compound or a pharmaceutically acceptable salt or a solvate thereof, and a synaptic vesicle protein 2A (SV2A) ligand.