Abstract

The age spectrum of human populations is shifting toward the older with larger proportions suffering physical decline. Mitochondria influence the pace of aging as the energy they provide for cellular function in the form of adenosine triphosphate (ATP) declines with age. Mitochondrial density is greatest in photoreceptors, particularly cones that have high energy demands and mediate color vision. Hence, the retina ages faster than other organs, with a 70% ATP reduction over life and a significant decline in photoreceptor function. Mitochondria have specific light absorbance characteristics influencing their performance. Longer wavelengths spanning 650–>1,000 nm improve mitochondrial complex activity, membrane potential, and ATP production. Here, we use 670-nm light to improve photoreceptor performance and measure this psychophysically in those aged 28–72 years. Rod and cone performance declined significantly after approximately 40 years of age. 670-nm light had no impact in younger individuals, but in those around 40 years and older, significant improvements were obtained in color contrast sensitivity for the blue visual axis (tritan) known to display mitochondrial vulnerability. The red visual axis (protan) improved but not significantly. Rod thresholds also improved significantly in those >40 years. Using specific wavelengths to enhance mitochondrial performance will be significant in moderating the aging process in this metabolically demanding tissue.

https://academic.oup.com/biomedgerontology/article/75/9/e49/5863431

Extract:

This pilot study has limitations due to its sample size, but the results reveal significant improvement in both rod and cone function in an aged cohort but not in younger individuals. This difference is presumably because age-related mitochondrial decline has not yet affected the younger individuals. Widespread positive results using long-wavelength light in aging and disease in animals have provided an impetus for their clinical application in full-scale clinical trials for diabetic retinopathy (NCT03866473) and age related macular degeneration (NCT02725762, 03878420). However, a recently published study on AMD patients has failed to show any improvement in retinal function in this disease (25). Consequently, there is much that we still need to understand regarding the advantages and limits of this therapeutic route. 

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Abstract

Purpose: Light is a salient cue that can influence neurodevelopment and the immune system. Light exposure out of sync with the endogenous clock causes circadian disruption and chronic disease. Environmental light exposure may contribute to developmental programming of metabolic and neurological systems but has been largely overlooked in Developmental Origins of Health and Disease (DOHaD) research. Here, we investigated whether developmental light exposure altered programming of visual and metabolic systems.

Methods: Pregnant mice and pups were exposed to control light (12:12 light:dark) or weekly light cycle inversions (circadian disruption [CD]) until weaning, after which male and female offspring were housed in control light and longitudinally measured to evaluate differences in growth (weight), glucose tolerance, visual function (optomotor response), and retinal function (electroretinogram), with and without high fat diet (HFD) challenge. Retinal microglia and macrophages were quantified by positive Iba1 and CD11b immunofluorescence.

Results: CD exposure caused impaired visual function and increased retinal immune cell expression in adult offspring. When challenged with HFD, CD offspring also exhibited altered retinal function and sex-specific impairments in glucose tolerance.

Conclusions: Overall, these findings suggest that the light environment contributes to developmental programming of the metabolic and visual systems, potentially promoting a pro-inflammatory milieu in the retina and increasing the risk of visual disease later in life.

https://pubmed.ncbi.nlm.nih.gov/33861321/

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See the image in the article: An intrinsically photosensitive retinal ganglion cell (ipRGC) as it would appear if you looked at a mouse’s retina through the pupil. The white arrows point to the many different types of cells it networks with: other subtypes of ipRGC cell (red, blue and green) and retinal cells that are not ipRGCs (red). The white bar is 50 micrometers long, approximately the diameter of a human hair. (Image by Franklin Caval-Holme)

By the second trimester, long before a baby’s eyes can see images, they can detect light.

But the light-sensitive cells in the developing retina — the thin sheet of brain-like tissue at the back of the eye — were thought to be simple on-off switches, presumably there to set up the 24-hour, day-night rhythms parents hope their baby will follow.

University of California, Berkeley, scientists have now found evidence that these simple cells actually talk to one another as part of an interconnected network that gives the retina more light sensitivity than once thought, and that may enhance the influence of light on behavior and brain development in unsuspected ways.

In the developing eye, perhaps 3% of ganglion cells — the cells in the retina that send messages through the optic nerve into the brain — are sensitive to light and, to date, researchers have found about six different subtypes that communicate with various places in the brain. Some talk to the suprachiasmatic nucleus to tune our internal clock to the day-night cycle. Others send signals to the area that makes our pupils constrict in bright light.

But others connect with surprising areas: the perihabenula, which regulates mood, and the amygdala, which deals with emotions.

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Babies in the womb may see more than we thought

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