The invention provides methods of treatment or prophylaxis of damaging effects of penetrative injury to the brain or other part of the central nervous system. The methods are based in part on results in a rodent model of penetrative ballistic injury showing that an inhibitor of PDF-95 NMDAR interaction is effective in inhibiting neurological deficits resulting from such injury. The methods are useful for treating subjects having or at risk of penetrative brain injury, including subjects who have been shot in the head or at risk of such injury (e.g., military or law enforcement personnel).

Compositions, pharmaceutical compositions and biodegradable pharmaceutical compositions containing at least one analog of spadin or at least one analog of a propeptides of spadin or mixtures thereof are described. Methods for treating depression using the analogs of spadin or analogs of propeptides of spadin or mixtures thereof, as well as methods for blocking TREK-1 channel activity are also disclosed.

Alpha-sheet polypeptide multimers, and polypeptides for making multimers, compositions and medical devices including them, and their use for treating and diagnosing amyloid diseases or amyloid-associated diseases are disclosed.

A peptide having an ED.sub.50 of less than 500 nm, in particular 10 nM to an antibody which recognizes an epitope on an extracellular 1 loop 2 or 2 loop1 of a human adrenoceptor wherein the antibody's binding to the epitope results in an increase of -secretase activity, an increased release of -amyolid molecules and/or cellular dysfunction of cerebral blood vessel cells, glia cells or neurons, wherein the ED.sub.50 value is measured by bioassay.

The present invention provides lyophilized formulations of active agents, particularly of TAT-NR2B9c. TAT-NR2B9c has shown promise for treating stroke, aneurysm, subarachnoid hemorrhage and other neurological or neurotraumatic conditions. Such formulations are stable at room temperature thus facilitating maintenance of supplies of such a formulation in ambulances for administration at the scene of illness or accident or in transit to a hospital.

The invention provides nucleic acids and nucleic acid expression vectors containing optimized mGluR6 promoters for expression of transgenes in the retina. The compositions and methods of the invention are useful for expression of gene products to preserve, improve, or restore phototransduction or vision.

Alpha-sheet polypeptide multimers, and polypeptides for making multimers, compositions and medical devices including them, and their use for treating and diagnosing amyloid diseases or amyloid-associated diseases are disclosed.

A composition and method for treatment of opioid use disorder (OUD) is provided by expressing a novel mu receptor mutant, LAMuOR (Low Affinity Mu Opioid Receptor), with reduced binding affinity for opioids such that it is activated only by the high concentration of exogenous opioids encountered in OUD but not by the low concentrations of endogenous opioids that occur physiologically. When expressed in specific brain circuits, these low-affinity mu opioid receptors can suppress reward-related neuronal activity specifically in the presence of opioids of abuse, thereby reducing abuse potential.

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.

Provided are compositions and method for prophylaxis and/or therapy of hearing loss or related dysfunctions, including but not limited to tinnitus, that could be ameliorated by restoring central nervous system inhibitory synapses. The compositions include polynucleotides and viral vectors that are used to express at least one GABA receptor component which may be a GABA.sub.A receptor alpha 1 subunit or GABAR receptor Ib subunit. Expression of the GABA receptor may be under control of a CaMKII promoter.