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Neuroprotective therapies for glaucoma.

Song W, Huang P, Zhang C - Drug Des Devel Ther (2015)

Bottom Line: However, it has been found that progressive GON is still present in some patients with effective IOP decrease.Therefore, risk factors other than IOP elevation, like neurotrophin deprivation and excitotoxicity, contribute to progressive GON.Novel approaches of neuroprotection may be more effective for preserving the function of the optic nerve.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Peking University Third Hospital, Beijing, People's Republic of China.

ABSTRACT
Glaucoma is the second leading cause for blindness worldwide. It is mainly caused by glaucomatous optic neuropathy (GON) characterized by retinal ganglion cell loss, which leads to visual field defect and blindness. Up to now, the main purpose of antiglaucomatous therapies has been to lower intraocular pressure (IOP) through surgeries and medications. However, it has been found that progressive GON is still present in some patients with effective IOP decrease. Therefore, risk factors other than IOP elevation, like neurotrophin deprivation and excitotoxicity, contribute to progressive GON. Novel approaches of neuroprotection may be more effective for preserving the function of the optic nerve.

No MeSH data available.


Related in: MedlinePlus

Excitotoxicity induced by excess glutamate.Notes: Extensive stimulation of NMDARs by glutamate leads to high level of Ca2+ to enter the cell, activating enzymes including phospholipases, endonucleases, and proteases. These enzymes may lead to apoptosis of the cell.Abbreviation: NMDAR, N-methyl-D-aspartic acid receptor.
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f3-dddt-9-1469: Excitotoxicity induced by excess glutamate.Notes: Extensive stimulation of NMDARs by glutamate leads to high level of Ca2+ to enter the cell, activating enzymes including phospholipases, endonucleases, and proteases. These enzymes may lead to apoptosis of the cell.Abbreviation: NMDAR, N-methyl-D-aspartic acid receptor.

Mentions: Excitotoxicity is the pathological process in neurons resulting from overactivation of N-methyl-D-aspartic acid receptors (NMDARs) by the excitatory neurotransmitter glutamate. The extensive stimulation of NMDARs allows high level of Ca2+ to enter the cell, activating enzymes including phospholipases, endonucleases, and proteases such as calpain. These enzymes may lead to the damage of plasma membrane, cytoskeleton, and DNA, and other cell components (Figure 3).27 Dreyer et al showed a twofold elevation in the glutamate level in the vitreous body of glaucoma patients, indicating the possibility of an excitotoxic mechanism resulting in RGC death.28 Accordingly, NMDAR blockers and calcium channel blockers (CCBs) can be used to inhibit excitotoxicity in RGCs and to delay GON progression and visual field loss in glaucoma patients.


Neuroprotective therapies for glaucoma.

Song W, Huang P, Zhang C - Drug Des Devel Ther (2015)

Excitotoxicity induced by excess glutamate.Notes: Extensive stimulation of NMDARs by glutamate leads to high level of Ca2+ to enter the cell, activating enzymes including phospholipases, endonucleases, and proteases. These enzymes may lead to apoptosis of the cell.Abbreviation: NMDAR, N-methyl-D-aspartic acid receptor.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4362661&req=5

f3-dddt-9-1469: Excitotoxicity induced by excess glutamate.Notes: Extensive stimulation of NMDARs by glutamate leads to high level of Ca2+ to enter the cell, activating enzymes including phospholipases, endonucleases, and proteases. These enzymes may lead to apoptosis of the cell.Abbreviation: NMDAR, N-methyl-D-aspartic acid receptor.
Mentions: Excitotoxicity is the pathological process in neurons resulting from overactivation of N-methyl-D-aspartic acid receptors (NMDARs) by the excitatory neurotransmitter glutamate. The extensive stimulation of NMDARs allows high level of Ca2+ to enter the cell, activating enzymes including phospholipases, endonucleases, and proteases such as calpain. These enzymes may lead to the damage of plasma membrane, cytoskeleton, and DNA, and other cell components (Figure 3).27 Dreyer et al showed a twofold elevation in the glutamate level in the vitreous body of glaucoma patients, indicating the possibility of an excitotoxic mechanism resulting in RGC death.28 Accordingly, NMDAR blockers and calcium channel blockers (CCBs) can be used to inhibit excitotoxicity in RGCs and to delay GON progression and visual field loss in glaucoma patients.

Bottom Line: However, it has been found that progressive GON is still present in some patients with effective IOP decrease.Therefore, risk factors other than IOP elevation, like neurotrophin deprivation and excitotoxicity, contribute to progressive GON.Novel approaches of neuroprotection may be more effective for preserving the function of the optic nerve.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Peking University Third Hospital, Beijing, People's Republic of China.

ABSTRACT
Glaucoma is the second leading cause for blindness worldwide. It is mainly caused by glaucomatous optic neuropathy (GON) characterized by retinal ganglion cell loss, which leads to visual field defect and blindness. Up to now, the main purpose of antiglaucomatous therapies has been to lower intraocular pressure (IOP) through surgeries and medications. However, it has been found that progressive GON is still present in some patients with effective IOP decrease. Therefore, risk factors other than IOP elevation, like neurotrophin deprivation and excitotoxicity, contribute to progressive GON. Novel approaches of neuroprotection may be more effective for preserving the function of the optic nerve.

No MeSH data available.


Related in: MedlinePlus