Novel agents for ameliorating motor disorder

Abstract

A novel medicament for treating neurodegenerative diseases, especially for ameliorating dyskinesia, comprising as an active ingredient selenoprotein P and / or a peptide fragment or a series of peptide fragments derived from said protein is provided. The novel medicament for treating neurodegenerative diseases, especially for ameliorating dyskinesia, according to the present invention is suitably applicable to diseases with decrease in motor function.

Description

TECHNICAL FIELD OF THE INVENTION [0001] The present invention relates to a novel use of plasma proteins, belonging to the field of medical drugs. More specifically, the present invention relates to a medicament for treating neurodegenerations caused by cell death or cellular degeneration of the cells consisting of the nervous system, such as aging, trauma, cerebrovascular disorders, immunopathy, ataxia, epilepsy, motor neuron disorders, and the like. Still more specifically, the present invention relates to a medicament for treating neurodegenerative disorders, especially for dyskinesia, comprising as an active ingredient selenoprotein P, one of plasma proteins, more preferably a peptide fragment or a series of peptide fragments derived from the C-terminal of selenoprotein P. BACKGROUND OF THE INVENTION [0002] Neural diseases, where cell death or cellular degeneration of the cells consisting of the nervous system such as neurocytes or glia cells are involved, include cerebrovascular...

AI Technical Summary

Benefits of technology

[0017] Under the circumstances, the present inventors have found that selenoprotein P, a protein derived from blood components, more preferably a peptide fragment from the C-terminal of selenoprotein P, exhibits a cell death-inhibitory activity, which hitherto has not been reported, and have filed a patent application (PCT / JP99 / 06322) for this finding. The present inventors further investigated for providing a novel medicament for ameliorating neurodegenerative diseases, especially for ameliorating dyskinesia. As a result, selenoprotein P or a peptide fragment or a series of peptide fragments derived from the C-terminal of selenoprotein P surprisingly proved to be efficacious as a medicament for ameliorating dyskinesia in humans or other animals as demonstrated in animal models which received in vivo administration thereof. Based on this finding, the present inventors have thus completed the present invention.

Problems solved by technology

Lesions in the vermis induce trunk ataxia, exhibits astasia-abasia, and gluteus maximus gait, yields difficulty in maintaining posture and position with disorder in balance.

As the aging process proceeds, man's physical function continually deteriorates.

For example, the proceedings of the aging process render the brain atrophic, in its extremity resulting in gait disability or dementia.

When a strong external pressure is applied in case of accidents, dislocation fracture of the spinal column occurs to press the spinal cord or to cause fractural injury in the spinal cord, resulting in injury of the spinal cord.

However, the system may sometimes act unfavorably against the living body.

The oxygen lack first provides with functional impairment via blockage of ATP production, then leads to degeneration, necrosis or atrophy.

Specifically, decrease in oxygen and glucose provisions due to ischemia triggers generation of free radicals, excess accumulation of glutamic acid, increase in intracellular calcium ion level, and enhancement of NO production, eventually resulting in death of neurocytes.

With these reasons, cell death or cellular degeneration of neurocytes can be the cause of dyskinesia.

However, these medicaments cannot entirely inhibit dyskinesia.

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