Researchers from Louisiana State University in New Orleans have discovered previously unknown gene interactions that are common to ischemic stroke [i.e., a stroke in which blood flow to a part of the brain is blocked] and age-related macular degeneration (AMD).
According to the research team, these gene interactions “make definitive decisions about whether a retina or brain cell will survive or die when threatened with disease onset” and thus could possibly prevent vision loss from AMD and promote recovery from a stroke.
Study author Dr. Nicolas Bazan states that “studying the eye and the brain might hold the key to creating therapeutic solutions for blindness, stroke, and other seemingly unrelated conditions associated with the central nervous system.”
From Cell Death & Differentiation
This neuroscience-based research has been published in the January 30, 2015 advance online edition of Cell Death & Differentiation, a peer-reviewed academic journal from Nature Publishing Group devoted to cell biology, molecular biology, and biochemistry. The authors are J. M. Calandria, A. Asatryan, V. Balaszczuk, E. J. Knott, B. K. Jun, P. K. Mukherjee, L. Belayev, and N. G. Bazan from the Neuroscience Center of Excellence, School of Medicine, Louisiana State University (LSU) Health Sciences Center in New Orleans.
About Age-Related Macular Degeneration
Age-related macular degeneration (AMD) is a gradual, progressive, painless deterioration of the macula, the small sensitive area in the center of the retina that provides clear central vision. It is the leading cause of vision loss for people aged 60 and older in the United States. According to the American Academy of Ophthalmology, 10-15 million individuals have AMD. Approximately 85-90% of affected persons have the “dry” type of AMD; 10-15% have the “wet” type.
Dry Macular Degeneration
The dry (also called atrophic) type of AMD affects approximately 85-90% of individuals with AMD. Its cause is unknown, it tends to progress more slowly than the wet type, and there is not – as of yet – an approved treatment or cure. “Atrophy” refers to the degeneration of cells in a portion of the body; in this case, the cell degeneration occurs in the retina.
In dry age-related macular degeneration, small white or yellowish deposits, called drusen, form on the retina, in the macula, causing it to deteriorate or degenerate over time.
A retina with drusen
Drusen are the hallmark of dry AMD. These small yellow deposits beneath the retina are a buildup of waste materials, composed of cholesterol, protein, and fats. Typically, when drusen first form, they do not cause vision loss; they are, however, a risk factor for progressing to vision loss.
Wet (Neovascular) Macular Degeneration
In wet, or exudative, macular degeneration (AMD), the choroid (a part of the eye containing blood vessels that nourish the retina) begins to sprout abnormal new blood vessels that develop into a cluster under the macula, called choroidal neovascularization (neo = new; vascular = blood vessels).
The macula is the part of the retina that provides the clearest central vision. Because these new blood vessels are abnormal, they tend to break, bleed, and leak fluid under the macula, causing it to lift up and pull away from its base. This damages the fragile photoreceptor cells, which sense and receive light, resulting in a rapid and severe loss of central vision.
About the Research
Excerpted from LSU Health New Orleans makes discovery key to preventing blindness and stroke devastation, via EurekAlert! Science News:
“During the last few years, [our] laboratory has been immersed in studying gene regulation,” [study author] Dr. Nicolas Bazan says. “We have uncovered a novel control that makes definitive decisions about whether a retina or brain cell will survive or die when threatened with disease onset. The gene mechanism that we discovered is the interplay of two genes turned on by the messenger Neuroprotectin D1 (NPD1).”
Age-related macular degeneration (AMD) is a devastating disease that targets the retina of [elderly persons] and destroys cells in charge of receiving photons and transferring light signals to the brain for decoding. The causal mechanisms of this disease remain elusive. The retinal pigment epithelium (RPE) is a single layer of cells that accomplishes multiple functions, such as providing survival molecules that prevent photoreceptors from dying.
[Editor’s note: The retinal pigment epithelium (RPE) is a specialized retinal tissue that plays a critical role in maintaining the equilibrium of all retinal processes. It is the pigmented layer of the retina, containing the deepest cells of the retina.]
The research team worked with human RPE cells and an experimental model of ischemic stroke. They discovered novel mechanisms in cells with the ability to activate pathways that cross-talk one to another and then assemble consolidated responses that decide cell fate.
The researchers found that NPD1, the cross-talk messenger, is produced on-demand in the brain and retina and that it [activates] a network of positive signals essential for the well-being of vision and cognition.
They showed that NDP1 [activity] governs key gene interactions decisive in cell survival when threatened by disease or injury, demonstrating that NPD1 protects photoreceptors and also promotes neurological recovery from the most frequent form of stroke in humans.
VisionAware will continue to report the results of this – and related – neurologically-based macular degeneration research as they become available.