Neurotherapeutic compositions

Abstract

Novel neuroprotectant compositions and methods are described. β-Lactamase inhibitors are used to prevent or reduce loss of neuronal cells and neuronal cell function in patients afflicted with or susceptible to disease states or conditions known to result in or cause neuronal tissue insult.

Description

CROSS REFERENCE TO RELATED APPLICATION [0001] This application is a continuation of Ser. No. 10 / 114,174, filed on Apr. 2, 2002, which is a divisional of Ser. No. 09 / 782,507, filed Feb. 13, 2001, now U.S. Pat. No. 6,426,342, which is a continuation-in-part of U.S. Ser. No. 09 / 640,363, filed Aug. 16, 2000, now U.S. Pat. No. 6,627,625, which claims priority to U.S. Provisional Applications Nos. 60 / 149,115, filed Aug. 16, 1999; 60 / 172,452, filed Dec. 17, 1999; 60 / 176,570, filed Jan. 18, 2000, and 60 / 194,534, filed Apr. 4, 2000.FIELD OF THE INVENTION [0002] This invention relates to a new use of inhibitors of bacterial β-lactamases. More particularly, this invention is directed to the use of β-lactamase inhibitors for preventing or reducing neuronal damage in patients suffering from or susceptible to disease states characterized by loss of neuronal cells or loss of neuronal cell function. BACKGROUND OF THE INVENTION [0003] Over excitation of NMDA receptor channel complexes on post-synapt...

AI Technical Summary

Benefits of technology

[0004] Accordingly, the present invention provides a surprisingly effective neuroprotective therapy. It is based on the discovery that compound capable of inhibiting the activity of bacterial β-lactamases (i.e., β-lactamase inhibitors) is, as well, a powerful neuroprotective agent. The invention thus provides a method for preventing neuronal damage or the progression of neuronal damage in a patient suffering from or susceptible to said damage, characterized generally as a loss of neuronal cells or a loss of neuronal cell function, such as that secondary to the occurrence of strokes, seizures, neural trauma, and a multiplicity of neuro-degenerative disease states of widely variant etiology.

Problems solved by technology

Over excitation of NMDA receptor channel complexes on post-synaptic neurons following excessive release of glutamic acid from synaptozones and glial cells results in massive calcium ion influx into neuronal cells leading to their death.