Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Apr 6:13:643685.
doi: 10.3389/fnagi.2021.643685. eCollection 2021.

Transneuronal Degeneration in the Brain During Glaucoma

Affiliations
Review

Transneuronal Degeneration in the Brain During Glaucoma

Mengling You et al. Front Aging Neurosci. .

Abstract

The death of retinal ganglion cells (RGCs) is a key factor in the pathophysiology of all types of glaucoma, but the mechanism of pathogenesis of glaucoma remains unclear. RGCs are a group of central nervous system (CNS) neurons whose soma are in the inner retina. The axons of RGCs form the optic nerve and converge at the optic chiasma; from there, they project to the visual cortex via the lateral geniculate nucleus (LGN). In recent years, there has been increasing interest in the dysfunction and death of CNS and retinal neurons caused by transneuronal degeneration of RGCs, and the view that glaucoma is a widespread neurodegenerative disease involving CNS damage appears more and more frequently in the literature. In this review, we summarize the current knowledge of LGN and visual cortex neuron damage in glaucoma and possible mechanisms behind the damage. This review presents an updated and expanded view of neuronal damage in glaucoma, and reveals new and potential targets for neuroprotection and treatment.

Keywords: RGC; brain; glaucoma; neurodegenerative disease; neurons.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling editor declared a shared affiliation with the authors at time of review.

Figures

Figure 1
Figure 1
Risk factors such as high intraocular pressure and ischemia can cause the activation of cell apoptosis, the increase of excitotoxicity, and the imbalance of neurotrophic pathway, which will eventually cause the death of RGC. In the neurotrophic pathway, blue represents the pathway through which neurotrophic factors function under normal conditions, and red represents the pathway through which RGC damage is caused by stimulation.
Figure 2
Figure 2
Schematic diagram of visual pathway, lateral geniculate body and visual cortex.
Figure 3
Figure 3
Anatomical depiction of retrograde and anterograde transsynaptic degeneration in the visual pathway. Retrograde trans-synaptic degeneration describes the process by which damage to the posterior visual pathway (black) results in subsequent retinal degeneration. Anterograde trans-synaptic degeneration describes the process by which retinal degeneration leads to subsequent degeneration of the posterior visual pathway.

References

    1. Agudo-Barriuso M., Villegas-Perez M. P., De Imperial J. M., Vidal-Sanz M. (2013). Anatomical and functional damage in experimental glaucoma. Curr. Opin. Pharmacol 13, 5–11. 10.1016/j.coph.2012.09.006 - DOI - PubMed
    1. Almasieh M., Wilson A. M., Morquette B., Cueva Vargas J. L., Di Polo A. (2012). The molecular basis of retinal ganglion cell death in glaucoma. Prog. Retin. Eye Res. 31, 152–181. 10.1016/j.preteyeres.2011.11.002 - DOI - PubMed
    1. Artero-Castro A., Rodriguez-Jimenez F. J., Jendelova P., Vanderwall K. B., Meyer J. S., Erceg S. (2020). Glaucoma as a neurodegenerative disease caused by intrinsic vulnerability factors. Prog Neurobiol. 193:101817. 10.1016/j.pneurobio.2020.101817 - DOI - PubMed
    1. Bourne R. R., Stevens G. A., White R. A., Smith J. L., Flaxman S. R., Price H., et al. (2013). Causes of vision loss worldwide, 1990-2010: a systematic analysis. Lancet Glob. Health 1, e339–349. 10.1016/S2214-109X(13)70113-X - DOI - PubMed
    1. Burgoyne C. F., Downs J. C., Bellezza A. J., Suh J. K., Hart R. T. (2005). The optic nerve head as a biomechanical structure: a new paradigm for understanding the role of IOP-related stress and strain in the pathophysiology of glaucomatous optic nerve head damage. Prog. Retin. Eye Res. 24, 39–73. 10.1016/j.preteyeres.2004.06.001 - DOI - PubMed

LinkOut - more resources