Topical brimonidine reduces collateral damage caused by laser photocoagulation for choroidal neovascularization

Ferencz, J. R.; Gilady, Gila; Harel, Orly; Belkin, Michael; Assia, Ehud I.

doi:10.1007/s00417-005-1160-7

Cited by 17 publications

(13 citation statements)

References 10 publications

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“…Furthermore, the ability of BMD to improve visual function is documented in rodent models of retinal disease. 35, 36, 37 …”

Section: Discussionmentioning

confidence: 99%

Non-amyloidogenic effects of α2 adrenergic agonists: implications for brimonidine-mediated neuroprotection

Nizari¹,

Guo²,

Davis³

et al. 2016

Cell Death Dis

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The amyloid beta (Aβ) pathway is strongly implicated in neurodegenerative conditions such as Alzheimer's disease and more recently, glaucoma. Here, we identify the α2 adrenergic receptor agonists (α2ARA) used to lower intraocular pressure can prevent retinal ganglion cell (RGC) death via the non-amyloidogenic Aβ-pathway. Neuroprotective effects were confirmed in vivo and in vitro in different glaucoma-related models using α2ARAs brimonidine (BMD), clonidine (Clo) and dexmedetomidine. α2ARA treatment significantly reduced RGC apoptosis in experimental-glaucoma models by 97.7% and 92.8% (BMD, P<0.01) and 98% and 92.3% (Clo, P<0.01)) at 3 and 8 weeks, respectively. A reduction was seen in an experimental Aβ-induced neurotoxicity model (67% BMD and 88.6% Clo, both P<0.01, respectively), and in vitro, where α2ARAs significantly (P<0.05) prevented cell death, under both hypoxic (CoCl2) and stress (UV) conditions. In experimental-glaucoma, BMD induced ninefold and 25-fold and 36-fold and fourfold reductions in Aβ and amyloid precursor protein (APP) levels at 3 and 8 weeks, respectively, in the RGC layer, with similar results with Clo, and in vitro with all three α2ARAs. BMD significantly increased soluble APPα (sAPPα) levels at 3 and 8 weeks (2.1 and 1.6-fold) in vivo and in vitro with the CoCl2 and UV-light insults. Furthermore, treatment of UV-insulted cells with an sAPPα antibody significantly reduced cell viability compared with BMD-treated control (52%), co-treatment (33%) and untreated control (27%). Finally, we show that α2ARAs modulate levels of laminin and MMP-9 in RGCs, potentially linked to changes in Aβ through APP processing. Together, these results provide new evidence that α2ARAs are neuroprotective through their effects on the Aβ pathway and sAPPα, which to our knowledge, is the first description. Studies have identified the need for α-secretase activators and sAPPα-mimetics in neurodegeneration; α2ARAs, already clinically available, present a promising therapy, with applications not only to reducing RGC death in glaucoma but also other neurodegenerative processes involving Aβ.

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“…Furthermore, the ability of BMD to improve visual function is documented in rodent models of retinal disease. 35, 36, 37 …”

Section: Discussionmentioning

confidence: 99%

Non-amyloidogenic effects of α2 adrenergic agonists: implications for brimonidine-mediated neuroprotection

Nizari¹,

Guo²,

Davis³

et al. 2016

Cell Death Dis

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“…Clinical studies have shown that topical brimonidine improved the visual outcome of patients undergoing laser treatment for classic extrafoveal or juxtafoveal choroidal neovascularization treatment [93] and that brimonidine, but not timolol, topical therapy, improved contrast sensitivity of glaucoma patients after 3 months of treatment [94].…”

Section: Brimonidinementioning

confidence: 99%

Neuroprotection in Glaucoma: Old and New Promising Treatments

Rusciano¹,

Pezzino²,

Mutolo

et al. 2017

Advances in Pharmacological Sciences

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Glaucoma is a major global cause of blindness, but the molecular mechanisms responsible for the neurodegenerative damage are not clear. Undoubtedly, the high intraocular pressure (IOP) and the secondary ischemic and mechanical damage of the optic nerve have a crucial role in retinal ganglion cell (RGC) death. Several studies specifically analyzed the events that lead to nerve fiber layer thinning, showing the importance of both intra-and extracellular factors. In parallel, many neuroprotective substances have been tested for their efficacy and safety in hindering the negative effects that lead to RGC death. New formulations of these compounds, also suitable for chronic oral administration, are likely to be used in clinical practice in the future along with conventional therapies, in order to control the progression of the visual impairment due to primary open-angle glaucoma (POAG). This review illustrates some of these old and new promising agents for the adjuvant treatment of POAG, with particular emphasis on forskolin and melatonin.

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“…Этот эффект не связан с гипотензивной активностью бримонидина. Авторы полагают, что им можно объяснить сохранение зрительных функций у лабораторных живот ных в экспериментальных моделях глаукомы [32][33][34].…”

Section: бримонидин как нейропротекторный препаратunclassified

Selective α2 agonists in the treatment of glaucoma: neuroprotective properties and impact on ocular blood flow

Kurysheva¹

2019

Vestn. oftal'mol.

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Глаукома-главная причина необратимой слепоты в мире. Среди препаратов, направленных на снижение офтальмотонуса, важное место занимает селективный α-2-агонист бримонидин. В данной части обзора рассматриваются важные свойства бримонидина, характеризующие его как прямой нейропротектор многопланового действия. Рассмотрено влияние бримонидина на глазной кровоток, подчеркивается его роль в поддержании нормальной ауторегуляции глазного кровообращения.

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Topical brimonidine reduces collateral damage caused by laser photocoagulation for choroidal neovascularization

Abstract: Topical brimonidine improves the visual outcome of laser-treated classic extrafoveal or juxtafoveal CNV, possibly by protecting the neuroretina against collateral damage caused by the laser treatment.

Cited by 17 publications

References 10 publications

Non-amyloidogenic effects of α2 adrenergic agonists: implications for brimonidine-mediated neuroprotection

Non-amyloidogenic effects of α2 adrenergic agonists: implications for brimonidine-mediated neuroprotection

Neuroprotection in Glaucoma: Old and New Promising Treatments

Selective α2 agonists in the treatment of glaucoma: neuroprotective properties and impact on ocular blood flow

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