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Alzheimer’s disease and glaucoma: Is there a causal relationship?
  1. P Wostyn1,
  2. K Audenaert2,
  3. P P De Deyn3,4
  1. 1
    Department of Psychiatry, PC Sint-Amandus, Beernem, Belgium
  2. 2
    Department of Psychiatry, Ghent University Hospital, Ghent, Belgium
  3. 3
    Department of Neurology and Memory Clinic, Middelheim General Hospital (ZNA), Antwerp, Belgium
  4. 4
    Laboratory of Neurochemistry and Behavior, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium
  1. Correspondence to Dr P Wostyn, Department of Psychiatry, PC Sint-Amandus, Reigerlostraat 10, 8730 Beernem, Belgium; wostyn.peter{at}skynet.be

Abstract

Evidence of a link between Alzheimer’s disease (AD) and glaucoma has emerged from studies showing that patients with AD may have a significantly increased rate of glaucoma occurrence. In addition, it has been reported that patients with AD exhibit optic nerve degeneration and loss of retinal ganglion cells. In spite of intensive research, the clinical and genetic relationships between AD and glaucoma remain obscure. It is unclear whether the clinical correlation between the two diseases might be due to shared risk factors or the influence of one disorder on the other. Interestingly, certain observations may provide a clue towards a better understanding of the high rate of comorbidity reported between AD and glaucoma. In this article, we hypothesise that there may be a causal relationship between AD and glaucoma that may be explained by decreased cerebrospinal fluid pressure (CSFP) in patients with AD. A very recent study reported the intriguing new observation that mean CSFP was 33% lower in subjects with primary open-angle glaucoma than that of non-glaucomatous controls. It was noted that this observation supports the concept that an abnormal high trans-lamina cribrosa pressure difference, whether the result of elevated intraocular pressure, reduced CSFP, or both, plays an important role in glaucomatous optic nerve damage. Interestingly, it was also reported that a substantial proportion of AD patients have very low CSFP. Therefore, we hypothesise that an abnormal high trans-lamina cribrosa pressure difference may explain why patients with AD have a greater risk for developing glaucoma.

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Footnotes

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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