Brimonidine, a drug which is used to treat open-angle glaucoma or ocular hypertension, may have potential as a treatment for Alzheimer’s disease, say researchers from University College London.
The common eye disease open-angle glaucoma occurs when optic nerve damage results in a progressive loss of the visual field and increased pressure in the eye.
In trials on rats, brimonidine (marketed under the brand names Alphagan and Alphagan-P), has been found to reduce the formation of amyloid proteins in the retina, which are believed to be linked to Alzheimer’s.
Because amyloid plaques can be seen in the retinas of people with Alzheimer’s, the researchers say the retina can be viewed as an extension of the brain that provides an opportunity to diagnose and track progression of Alzheimer’s.
Brimonidine Reduced Neurodegeneration
Brimonidine was found to reduce neurodegeneration of cells in the retina by cutting the levels of beta amyloid in the eye. This was achieved by using the drug to stimulate the production of an alternative non-toxic protein which does not kill nerve cells.
Brimonidine acts through the activation of a G protein-coupled receptor, inhibiting the activity of adenylate cyclase. This reduces cAMP and hence aqueous humour synthesis by the ciliary body. Brimonidine also treats reddened skin by causing narrowing of blood vessels.
Study leader Professor Francesca Cordeiro, of the UCL Institute of Ophthalmology, said:
“The findings of our study could not have come at a more significant and important moment, given the increased prevalence of Alzheimer’s disease. As we live longer, there will be increasing demand for therapies that can help challenge this extremely damaging disease and we believe that our findings can make a major contribution."
The researchers hope that the drug will have a similar effect on the brain, although this was not tested in the current study.
Shereen Nizari et al
Non-amyloidogenic effects of α2 adrenergic agonists: implications for brimonidine-mediated neuroprotection
Cell Death and Disease (2016). DOI: 10.1038/cddis.2016.397
Last Updated on November 11, 2023