European journal of ophthalmology · 2001
Neuroprotection as a treatment for glaucoma: pharmacological and immunological approaches.
СтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Schwartz M
Аннотация
PURPOSE: Primary open-angle glaucoma is a chronic, progressive optic neuropathy associated with a gradual decline in visual functions, which may lead to blindness.
METHODS: In most cases, the optic neuropathy is associated with increased intraocular pressure. However, it is now generally accepted, that normalization of pressure, although necessary, is often not sufficient as a remedial measure. This is because of the existence of additional risk factors, some of which emerge as a consequence of the initial damage. This situation is reminiscent of the response to a traumatic axonal insult: some of the damage is immediate and is caused by the insult itself, while some is secondary and is caused by a deficiency of growth-supportive factors as well as by toxic factors derived from the damaged tissue. Accordingly, we have suggested that glaucoma may be viewed as a neurodegenerative disease and consequently is amenable to any therapeutic intervention applicable to these diseases.
CONCLUSIONS: There is evidence that neuroprotection can be achieved both pharmacologically and immunologically. Pharmacological intervention (e.g. by using selective alpha-2 adrenergic receptor agonists) neutralizes some of the effects of the nerve-derived toxic factors and possibly increases the ability of the remaining healthy neurons, at any given time, to cope with the stressful conditions. Immunological intervention boosts the body's own repair mechanisms for counteracting the toxicity of physiological compounds acting as stress signals.
METHODS: In most cases, the optic neuropathy is associated with increased intraocular pressure. However, it is now generally accepted, that normalization of pressure, although necessary, is often not sufficient as a remedial measure. This is because of the existence of additional risk factors, some of which emerge as a consequence of the initial damage. This situation is reminiscent of the response to a traumatic axonal insult: some of the damage is immediate and is caused by the insult itself, while some is secondary and is caused by a deficiency of growth-supportive factors as well as by toxic factors derived from the damaged tissue. Accordingly, we have suggested that glaucoma may be viewed as a neurodegenerative disease and consequently is amenable to any therapeutic intervention applicable to these diseases.
CONCLUSIONS: There is evidence that neuroprotection can be achieved both pharmacologically and immunologically. Pharmacological intervention (e.g. by using selective alpha-2 adrenergic receptor agonists) neutralizes some of the effects of the nerve-derived toxic factors and possibly increases the ability of the remaining healthy neurons, at any given time, to cope with the stressful conditions. Immunological intervention boosts the body's own repair mechanisms for counteracting the toxicity of physiological compounds acting as stress signals.