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Editors Selection IGR 11-3

Basic Research: Elevated CSF pressure and elevated IOP

Comment by George Lambrou on:

25731 Alzheimer's disease: Cerebral glaucoma?, Wostyn P; Audenaert K; De Deyn PP, Medical Hypotheses, 2010; 74: 973-977

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Could Alzheimer's Disease (AD) be the cerebral counterpart of POAG? Or, conversely, could some forms of POAG be the ocular counterpart of AD, as the mirror-title of a 2003 paper suggested (McKinnon SJ. Glaucoma: Ocular Alzheimer's Disease)? It is true that a number of analogies exist between the two conditions and that literature has accumulated in the last fifteen years exploring this hypothetical link. Wostyn et al. (836) review the most important findings and attempt to synthesize them into a coherent hypothesis, namely that an increase in intracranial pressure (ICP) may predispose a person to developing AD, not unlike the way an increase in IOP constitutes a risk factor for developing POAG. It is of interest that one of the authors had already formulated an early version of this hypothesis in a 1994 paper, published in the same journal.

Could an increase in intracranial pressure predispose a person to Alzheimer's disease, not unlike the way an increase in IOP constitutes a risk factor for developing POAG?

The arguments marshaled to support the hypothesis are mostly indirect. This is not surprising, since there is no straightforward non-invasive method to measure ICP: any such attempt involves a spinal tap! Thus, most evidence stems either from animal research or from clinical studies evaluating invasive procedures, like shunting of cerebrospinal fluid (CSF) in AD suspects. One such study in 181 patients had shown that a small percentage (ca. 4%) had abnormally high ICP. (Of note, however, another 24% had abnormally low ICP.) In diseases with impaired CSF circulation, like pseudotumor cerebri (a.k.a. benign intracranial hypertension), which is not linked to AD, or in normal-pressure hydrocephalus (characterized by increased resistance to CSF outflow and therefore its reduced turnover) which can be, changes have been observed in CSF levels of -amyloid and tau proteins, i.e., the constituents of the plaques and tangles characteristic of AD. Interestingly similar changes ‐ reduced levels of -amyloid and increased levels of tau ‐ have been observed in the vitreous of patients with glaucoma and diabetic retinopathy, suggesting some commonality in the neurodegenerative process. The sum total of this evidence is, however, inconclusive and ‐ as the authors themselves conclude ‐ their hypothesis remains highly speculative at this stage. Further studies will be necessary to elucidate whether glaucoma and AD share indeed some common pathogenic mechanism or whether the observed similarities are by-products of the neurodegenerative process.

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