期刊
ANNUAL REVIEW OF NEUROSCIENCE, VOL 35
卷 35, 期 -, 页码 153-179出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev.neuro.051508.135728
关键词
optic nerve head; ocular hypertension; astrocytes; retinal ganglion cells; glia
资金
- NATIONAL EYE INSTITUTE [R01EY012223, R29EY011721, P30EY016665, R01EY021525, R29EY012223, R01EY011721] Funding Source: NIH RePORTER
- Howard Hughes Medical Institute Funding Source: Medline
- NEI NIH HHS [R01 EY012223, EY021525, R01 EY021525, EY012223, P30 EY016665, EY011721] Funding Source: Medline
Glaucoma is a complex neurodegenerative disorder that is expected to affect 80 million people by the end of this decade. Retinal ganglion cells (RGCs) are the most affected cell type and progressively degenerate over the course of the disease. RGC axons exit the eye and enter the optic nerve by passing through the optic nerve head (ONH). The ONH is an important site of initial damage in glaucoma. Higher intraocular pressure (IOP) is an important risk factor for glaucoma, but the molecular links between elevated IOP and axon damage in the ONH are poorly defined. In this review and focusing primarily on the ONH, we discuss recent studies that have contributed to understanding the etiology and pathogenesis of glaucoma. We also identify areas that require further investigation and focus on mechanisms identified in other neurodegenerations that may contribute to RGC dysfunction and demise in glaucoma.
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