ELOVL2 Is A Critical Cell Survival Gene
Our science is based on breakthrough research conducted at the Shiley Eye Institute at the University of California San Diego and exclusively licensed to Visgenx. The research identified the critical role of ELOVL2 gene expression for maintaining the function and survival of cells in retina and other tissues and how its dysregulation may promote cellular aging / senescense.
Age-Related Decline of ELOVL2
DNA methylation is a process used by cells to regulate gene expression. Multiple studies have demonstrated ELOVL2 becomes increasingly methylated as cells age with a corresponding down regulation of expression.
Down Regulation of ELOVL2 Expression Contributes to Accelerated Aging in Ocular Tissues
As a consequence of ELOVL2 downregulation, there is a decrease in cellular levels of the lipid molecules it produces. Without adequate levels of these lipids in ocular tissues there is a:
- Decline in retinal pigmented epithelium (RPE) cell function
- Loss of photoreceptor cells
- Increased infiltration of inflammatory molecules
- Decline in visual function
Down Regulation of ELOVL2 Expression May Underlie Other (Non Ocular) Aging Related Disorders
Recent research suggests that declining ELOVL2 expression may not only underlie Age-Related Macular Degeneration but other disorders associated with aging including:
- Dementia / Alzheimers
ELOVL2 Functional Knock Out Mice
In mice, knockout of the ELOVL2 gene results in characteristic pathologies associated with AMD including: marked acceleration of drusen formation, complement infiltration (data not shown), and reduced visual response (ERG) compared to age matched wild type mice (WT).
Therapies in Focus.
Our strategy to slow cellular senescense in macular degeneration and other age-related disorders by “turning back the clock” to a more youthful level of ELOVL2 expression.