Condition focus: Optic Nerve & Mitochondrial Dysfunction
Mitochondrial optic neuropathies, including Leber’s hereditary optic neuropathy (LHON), result from mitochondrial dysfunction leading to retinal ganglion cell death and irreversible vision loss. This study investigated whether 670 nm near-infrared light could protect against optic nerve damage in a rotenone-induced mitochondrial dysfunction model. Rats received intravitreal rotenone injections to induce mitochondrial complex I inhibition, with experimental groups receiving 670 nm LED treatment before and after toxic insult.
Animals treated with 670 nm light demonstrated significant preservation of retinal ganglion cell function and survival compared to rotenone-only controls. Visual evoked potential recordings showed maintained electrical activity in treated animals versus severe deficits in untreated controls. Histological analysis revealed reduced retinal ganglion cell loss and preservation of optic nerve integrity. The protective effect was associated with enhanced mitochondrial enzyme activity and reduced oxidative stress markers. The findings establish proof-of-concept that 670 nm photobiomodulation can rescue mitochondrial function in optic neuropathy models, suggesting therapeutic potential for hereditary and acquired mitochondrial optic nerve diseases.
WaveFront Alignment:
Rojas’s demonstration that 670 nm rescues mitochondrial dysfunction in optic neuropathy validates the Spectral WaveFront’s wavelength selection for neuroprotection and supports its potential application in mitochondrial-based optic nerve diseases including LHON and other optic neuropathies.
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Editor’s note: Rojas 2008 establishes 670 nm neuroprotection in mitochondrial optic neuropathy models. For related optic nerve applications, see Szymanski 2013 and Fitzgerald 2010. Mitochondrial mechanisms appear in Beirne 2017 and Gkotsi 2014. Wavelength comparison in Giacci 2014.
Related Articles
- 670nm Light in Optic Nerve Injury – Szymanski 2013
- NIR Reduces Oxidative Stress in Optic Nerve Injury – Fitzgerald 2010
- Photostimulation of Mitochondria for Retinal Neurodegeneration – Beirne 2017
- Recharging Mitochondrial Batteries in Old Eyes – Gkotsi 2014
- 670nm vs 830nm: Comparative Neuroprotection – Giacci 2014
Key Takeaways
- 670 nm treatment preserved retinal ganglion cell function and survival in mitochondrial dysfunction model
- Visual evoked potentials maintained in treated animals versus severe deficits in rotenone-only controls
- Histological analysis showed reduced RGC loss and preserved optic nerve integrity
- Protective effect associated with enhanced mitochondrial enzyme activity and reduced oxidative stress
Study Overview
| Study Type: | Animal model (mitochondrial optic neuropathy) |
| Wavelength(s): | 670 nm (near-infrared) |
| Treatment Protocol: | LED treatment before and after rotenone-induced mitochondrial dysfunction |
| Sample Size: | Rat models with electrophysiology and histological assessment |
| Primary Outcome: | Significant RGC preservation and maintained visual evoked potentials versus controls |
Full Citation
Rojas JC, et al. (2008). Neuroprotective effects of near-infrared light in an in vivo model of mitochondrial optic neuropathy. J Neurosci, 28(50):13511-13521. View Publication
