Summary

Alzheimer's disease patients may be at a high risk of developing glaucoma. Drs. De Deyn, Van Dam, and colleagues are studying the underlying disease mechanisms responsible for this higher risk, both in patients and in mice engineered to have Alzheimer's disease (AD). These investigators hypothesize that reduced pressure in the liquid that surrounds the brain and spine, called cerebrospinal fluid, may be a major factor in this process.

Project Details

Drs. De Deyn, Van Dam, and colleagues will study the disease mechanisms underlying the link between Alzheimer's disease and increased risk of glaucoma, both in patients and in a mouse model. They propose that reduced cerebrospinal fluid (CSF) pressure and a high eye pressure (called a trans-lamina cribrosa pressure gradient) in the eye play an important role in the development of glaucoma in Alzheimer's disease patients.

These researchers will also evaluate whether brain shrinkage, typical for Alzheimer's disease, could be the cause of the reduced CSF pressure. In parallel, they will determine whether mice engineered to have Alzheimer's disease also have glaucoma, and, if so, will determine the underlying disease mechanisms.

This is the first clinical study set up to look at the link between Alzheimer's disease and glaucoma. The study of animals with Alzheimer's disease gives the opportunity to more easily study disease mechanisms at various stages of the disease.

If confirmed, these hypotheses could have remarkable implications in clinical practice. Careful attention by the clinician should be given to the potential for glaucoma in AD patients. Moreover, measurement of CSF pressure could be a monitoring tool in AD patients. Further research could raise some interesting possibilities for therapy. A randomized clinical trial could be recommended to test whether one could prevent the development of glaucoma in AD by manipulating CSF pressure. The use of a valid mouse model for AD would also allow for focused translational research and further insight into underlying pathophysiological mechanisms.