No one wants to be sick. No one wants to get a disease, especially diseases like Alzheimer’s and glaucoma. Glaucoma robs a person of his or her sight. Alzheimer’s robs a person of his or her mind. Interestingly enough, people who have Alzheimer’s are more likely to have glaucoma. They are both diseases that affect people over the age of 50, are chronic and they involve the loss of certain types of neurons.
While several studies have shown that people with glaucoma don’t have an increased risk of getting Alzheimer’s, a French study demonstrated that glaucoma patients were four times more likely to develop dementia. In particular, people with low-tension glaucoma were most at risk of getting dementia. People with Alzheimer’s and glaucoma both experience thinning of the retinal nerve fiber layer and loss of the retinal ganglion cells that make up the optic nerve. In addition, tau protein, another feature of Alzheimer’s, has been found in the vitreous jelly, the clear substance that fills the space in the eye from the lens to the back of the eye.
Currently, the research is inconclusive as to whether patients with open-angle glaucoma have an increased risk of developing dementia. Yet, there is other research going on that may lead to treatments for both Alzheimer’s and glaucoma. Scientists at Vanderbilt University Medical Center in Nashville, Tennessee, led by David Calkins, PhD, have found that when one optic nerve is damaged, the opposite optic nerve helps by sharing its metabolic energy. This sounds great, the problem is that doing this leads to more metabolic stress, which leads to neurodegeneration that spreads to other brain regions.
Researchers learned that when one optic nerve was stressed by a rise in intraocular pressure, glycogen was transferred from a healthy optic nerve to the stressed one. The energy is transferred from the optic nerve, across the optic chiasm, (an X-shaped structure formed by the crossing of the optic nerves) in the brain and down the other eye. It doesn’t sound like much, but it is a large distance that the glycogen has to travel.
The transfer is dependent on a protein known as connexin 43 (Cx43). This is a protein that makes up the astrocytes, which are star-shaped glial cells that store glycogen and release it as glucose. The gap junction are channels that connect cells and allow for the exchange of molecules, like glycogen, between them. The Cx43 was genetically eliminated in a mouse model, so the energy transfer didn’t happen.
While the energy sharing helps the diseased tissue in the short run, the tissue that is giving away the energy ends up more open to injury. This research suggests that targeting the astrocytes to reprogram them to make and store more glycogen to share with the neurons could be used to develop treatments for both Alzheimer’s and glaucoma.
While the jury is out on whether or not people with Alzheimer’s are more likely to get glaucoma and vice versa, scientists are learning more about cellular mechanisms that affect both, which can lead to treatments for both.