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Editors Selection IGR 8-2

Basic Research: Elevated CSF pressure and elevated IOP

Comment by Stuart McKinnon on:

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

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Wostyn et al. (836) have elucidated a hypothesis that elevated cerebrospinal fluid pressure (CSFP) may be responsible for the development of Alzheimer's disease (AD), in a manner analogous to the development of glaucoma due to elevated intraocular pressure (IOP). The authors note that the optic nerve and eye are embryologically derived from the third ventricle, and that both IOP and intracranial pressure have similar pressure ranges and responses to changes in intrathoracic and intraabdominal pressure. The authors hypothesize that elevated CSFP is related to decreased choroidal plexus secretion of CSF leading to decreased clearance of toxic metabolites including amyloid-beta and tau, which are implicated in the pathogenesis of AD. The authors cite a 2006 study by Silverberg et al,¹ in which opening CSFP was measured in 181 subjects with a diagnosis of AD. One hundred and seventy-four subjects (96.1%) with AD had a mean opening CSFP of 103 ± 47 mm H₂O, which was significantly lower than a control group of subjects with Parkinson's disease (140 ± 60 mm H₂O). The authors also noted that there is no published report of an association between AD and pseudotumor cerebri (PTC), a condition associated with elevated CSFP. The authors argue that in PTC, low CSF protein levels are noted, implying rapid metabolism of potential toxic metabolites which would preclude the development of AD in this situation. These findings appear to contradict the author's hypothesis of a causal relationship between elevated CSFP and the development of AD. As the authors point out, the development of animal models of elevated CSFP would allow for the assessment of the development of AD-like pathology, and help to provide evidence for this intriguing yet unsupported hypothesis.

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