Antiphosphatidylserine antibodies are elevated in normal tension glaucoma

Kremmer, Stephan; Kreuzfelder, E.; Klein, Reinhild; Bontke, N.; Henneberg-Quester, K B; Steuhl, Klaus‐Peter; Grosse‐Wilde, H.

doi:10.1046/j.1365-2249.2001.01578.x

Cited by 66 publications

(33 citation statements)

References 17 publications

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“…Additional recent reports from several laboratories of elevated serum antibodies against neuron-specific enolase [27] or phosphatidylserine [28], and complex patterns of serum antibodies against retina and optic nerve antigens [29] in glaucoma patients also support the association of serum autoantibodies with glaucomatous neurodegeneration.…”

Section: Humoral Immune Responsementioning

confidence: 75%

Glaucoma

Tezel

Wax

2007

Chemical Immunology and Allergy

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Glaucoma is a chronic neurodegenerative disease of the optic nerve, in which apoptosis of retinal ganglion cells (RGCs) and progressive loss of optic nerve axons result in structural and functional deficits in glaucoma patients. This neurodegenerative disease is indeed a leading cause of blindness in the world. The glaucomatous neurodegenerative environment has been associated with the activation of multiple pathogenic mechanisms for RGC death and axon degeneration. Growing evidence obtained from clinical and experimental studies over the last decade also strongly suggests the involvement of the immune system in this neurodegenerative process. Paradoxically, the roles of the immune system in glaucoma have been described as either neuroprotective or neurodestructive. A balance between beneficial immunity and harmful autoimmune neurodegeneration may ultimately determine the fate of RGCs in response to various stressors in glaucomatous eyes. Based on clinical data in humans, it has been proposed that one form of glaucoma may be an autoimmune neuropathy, in which an individual's immune response facilitates a somatic and/or axonal degeneration of RGCs by the very system which normally serves to protect it against tissue stress.

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Section: Humoral Immune Responsementioning

confidence: 75%

Glaucoma

Tezel

Wax

2007

Chemical Immunology and Allergy

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“…This might explain the higher frequency of thromboembolism in NTG patients and suggests a strong association of apoptosis or circulatory disturbances and NTG. 78 However, in another study investigating the association between NTG and autoantibodies detected in rheumatic disease, NTG patients did not show elevated levels of such antibodies, but only a higher level of antiprothrombin antibodies relative to the POAG group. 79 The possible pathogenic role of Helicobacter pylori in increased autoimmunity has been raised as a secondary aggravating factor for NTG.…”

Section: Autoimmunitymentioning

confidence: 88%

“…19,77 Patients with NTG also showed increased antiphosphatidylserine antibodies compared with POAG patients and control subjects. 78 These antibodies bind to phosphatidylserine molecules, which are shifted from the inner to the outer leaflet of cell membranes. This process activates the coagulation cascade and thus can cause thrombosis.…”

Section: Autoimmunitymentioning

confidence: 99%

Update on the Prevalence, Etiology, Diagnosis, and Monitoring of Normal-Tension Glaucoma

Kim

Park²

2016

Asia-Pacific Journal of Ophthalmology

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Glaucoma is a leading cause of blindness worldwide. Normal-tension glaucoma (NTG) is a type of open-angle glaucoma with intraocular pressure measurements always 21 mm Hg or less. A controversy surrounding NTG is the question of whether it should be regarded as a disease within the spectrum of primary open-angle glaucoma or as a distinctive disease entity. Nonetheless, NTG does have distinctive features compared with primary open-angle glaucoma: intraocular pressure-independent risk factors for development of NTG, characteristic patterns of structural and functional damage, and a unique disease course. This review provides an overview and update on the current issues surrounding the prevalence, etiology, diagnosis, and monitoring of NTG.

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“…anti-GFAP, anti-14-3-3) could be detected in glaucoma patients. (59)(60)(61)(62)(63)(64)(65)(66)(67)(68) However, whether the autoantibodies have a causative effect or appear as an epiphenomenon of the disease is yet to be unraveled. The downregulations are possibly related to a loss of natural protective autoimmunity and a disbalance of naturally occurring autoantibodies promoting neurodegenerative processes.…”

Section: Autoimmune Biomarkersmentioning

confidence: 99%

Biomarkers and surrogate endpoints in the glaucomatous optic neuropathy: new developments and a review

Kasahara¹

2015

Revista Brasileira De Oftalmologia

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Glaucoma is a group of progressive optic neuropathies that have in common a slow progressive degeneration of retinal ganglion cells and their axons, resulting in a distinct RESUMOO glaucoma compreende um grupo de neuropatias ópticas progressivas que tem em comum a degeneração lenta e progressiva das células ganglionares e seus axônios, resultando em aparência única do disco óptico e, simultaneamente, um padrão correspondente de perda visual. Biomarcadores são características medidas objetivamente e avaliadas como indicadores de processo biológico normal, processos patológicos ou respostas farmacológicas à uma intervenção terapêutica. Vários marcadores biológicos foram associados com glaucoma, especialmente os genéticos, proteômicos, autoimunes e outros biomarcadores moleculares, embora a maioria ainda necessite de validação clínica. Existem potenciais benefícios em usar biomarcadores. Informações podem ser obtidas mais precocemente, de forma mais rápida e menos onerosa. Esta revisão resume os últimos avanços e métodos em biomarcadores de glaucoma e seu possível uso no diagnóstico, estadiamento e como preditores da resposta ao tratamento.

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Antiphosphatidylserine antibodies are elevated in normal tension glaucoma

Cited by 66 publications

References 17 publications

Glaucoma

Glaucoma

Update on the Prevalence, Etiology, Diagnosis, and Monitoring of Normal-Tension Glaucoma

Biomarkers and surrogate endpoints in the glaucomatous optic neuropathy: new developments and a review

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