Alzheimer's hits glaucoma between the eyes
protein associated with Alzheimer's disease to glaucoma, opening up
a much needed new target for glaucoma therapies.
The latest research, published in an early view article in the US journal, Proceedings of the National Academy of Science, has found that beta amyloid proteins, commonly associated with Alzheimer's disease, are also found in the optic nerves of rats suffering from glaucoma and that certain Alzheimer's drugs can prevent this build up. This latest research could provide hope for the 65m people suffering from glaucoma worldwide as well as the 18m people that suffer from dementia by providing further information about the progression of the two diseases. Little is known about what causes glaucoma and the damage the disease causes to the optic nerve in the eye, although the build up of pressure on the eye has been traditionally implicated. Clinical treatments try to reduce this 'intraocular pressure', however at least 10 per cent of patients who receive treatment still develop blindness. The researchers from the UK's University College London (UCL) Institute of Opthalmology, developed a technique for visualising nerve cell damage in the retina, known as Detection of Apoptosin Retinal Cells (DARC), and used it to demonstrate that beta amyloid build up leads to retinal nerve cell death. "We've seen for the first time that there is a clear link between what causes Alzheimer's disease and one of the basic mechanisms behind glaucoma," said Dr Francesca Cordeiro, lead author of the study. The researchers hypothesise that the stress caused by during glaucoma progression causes the release of beta amyloid into the eye leading to nerve cell death. "If you look at all the diseases where beta amyloid has been found, such as Alzheimer's, Parkinson's, Huntington's etc, they are all neurodegenerative disorders where the nerve cells are under stress and eventually die," said Dr Cordeiro. By using a rat glaucoma model, the researchers were able to show that raising the pressure on the eye caused beta amyloid to be released and cause nerve cell death. The researchers then tested three Alzheimer's therapies on the glaucoma model: a beta amyloid antibody, Bapineuzumab, which is currently in Phase III development by Wyeth and Elan; as well as Congo Red which is known to inhibit beta amyloid aggregation; and beta-Secretase Inhibitor which reduces the formation of beta amyloid. The antibody therapy was found to be the most effective of the three monotherapies, but a combination of three worked even better. Dr Cordeiro heralded the success as a "brand new treatment strategy". Not only did the research offer new hope for glaucoma sufferers, but the DARC technique should also allow researchers to study the effectiveness of new Alzheimer's drugs faster than the currently used MRI (magnetic resonance imaging) and PET (positron emission tomography) techniques. "If there is this commonality [between glaucoma and Alzheimer's] then imaging the eye would be a very good way of detecting Alzheimer's in a patient as well as monitoring treatment effectiveness," said Professor Tom Salt, also of UCL and one of the contributing authors.
