Retinal degenerative diseases include a wide spectrum of conditions, ranging from rare inherited disorders to common multifactorial diseases such as age-related macular degeneration (AMD), one of the leading causes of blindness in developed countries. Increasing evidence indicates that impaired autophagy \u2014 the cellular process responsible for removing damaged components \u2014 plays a key role in the development and progression of these conditions.<\/p>\n\n\n\n
In the degenerative process, damage typically begins in the outer retina, particularly within the retinal pigment epithelium (RPE), and then progressively extends to the inner retinal layers, ultimately affecting the entire retina.<\/p>\n\n\n\n
Among the proteins involved in autophagy, Beclin1 appears to play a crucial role in maintaining retinal integrity. This protein acts at the intersection of several cellular clearance pathways, including mitophagy, lipophagy, and glycophagy, all of which are essential for retinal health and are often disrupted in degenerative diseases.<\/p>\n\n\n\n
In this study, we investigated the effects of reduced Beclin1 expression using an aged mouse model carrying a single functional copy of the BECN1 gene. Molecular analyses confirmed a significant decrease in both Beclin1 gene expression and protein levels across the retina.<\/p>\n\n\n\n
Using a combination of histological, molecular, and imaging techniques, we observed a marked degeneration of the retinal pigment epithelium and photoreceptor layers, including the disruption of tight junction proteins that are essential for maintaining retinal structure and function. Degeneration also extended to the inner retinal layers, where an increase in the neurodegenerative protein alpha-synuclein was detected alongside impaired autophagy markers.<\/p>\n\n\n\n
Overall, these findings highlight the essential role of Beclin1 in preserving retinal structure and function, and demonstrate how its reduction leads to a progressive, multi-layered retinal degeneration.<\/p>\n\n\n\n
Importantly, the study also supports the potential of photobiomodulation (PBM)<\/strong> \u2014 the use of specific wavelengths of light \u2014 to enhance Beclin1 activity and support retinal health, suggesting a promising, non-invasive therapeutic approach targeting the underlying cellular mechanisms of retinal degeneration.<\/p>\n\n\n\n <\/p>\n\n\n\n