Alzheimer's disease

Can chronic increased intracranial pressure or exposure to repetitive intermittent intracranial pressure elevations raise your risk for Alzheimer’s disease?

Author: Wostyn P

Over a decade ago, I formulated the hypothesis that cumulative effects of exposure to high intracranial pressure (ICP) may contribute to the development of Alzheimer's disease (AD), though not necessarily in an exclusive way. In addition to individual ICP characteristics (high 'physiological' ICP) and diseases causing ICP elevation, various activities with significant Valsalva effort, such as weightlifting and wind instrument playing, can generate very high ICPs. Recent studies of normal-pressure hydrocephalus (NPH), glaucoma and Alzheimer's disease provide supportive evidence for this hypothesis. A number of studies have shown a high incidence of AD related lesions in patients with NPH, which is known to be associated with prolonged elevation of ICP in a majority of cases. In both NPH and AD, an important decrease in cerebrospinal fluid (CSF) production was calculated. According to researchers in the US, the resulting CSF stagnation with impaired clearance and accumulation of neurotoxic substances may play an important role in the onset and progression of AD. They tested the hypothesis that improving CSF turnover by means of an investigational low-flow ventriculoperitoneal shunt will delay the progression of dementia in patients with Alzheimer's disease. With regard to the observed decrease in CSF production in patients suffering from NPH, it was postulated that chronic increased ICP causes downregulation of CSF production. It is hypothesized here that repetitive intermittent ICP elevations also may lead to downregulation of CSF production due to long-term cumulative effects. If the latter proves to be true, then both chronic increased ICP and repeated exposures to increased ICP (e.g., repetitive Valsalva maneuvers) may cause a similar cascade of CSF circulatory failure events leading to AD over time. Furthermore, AD may be causally related to increased ICP through other pathomechanisms. Additional supportive evidence for the role of a pressure factor in the pathogenesis of AD comes from studies concerning glaucoma. Elevated intraocular pressure (IOP) is a hallmark of glaucoma. Recently, similarities in pathophysiology between glaucoma and AD have been noted, with increased processing of amyloid precursor protein (APP) and up-regulation of beta-amyloid protein expression in retinal ganglion cells (RGCs). Given this link between AD and glaucoma, evidence for a causal relationship between repetitive intermittent ICP elevations and AD is gained from research indicating that high resistance wind instrument playing raises IOP and may result in glaucomatous damage. To test the validity of the hypothesis that exposure to repetitive but nonsustained ICP elevations may predispose to AD a non-invasive, epidemiological study is proposed in this paper.

Mild traumatic brain injury: a risk factor for neurodegeneration

Authors: Brandon E Gavett 1,2, Robert A Stern 1,2, Robert C Cantu 2,3,4, Christopher J Nowinski 2,3 and Ann C McKee 1,2,5,6 *.

Recently, it has become clear that head trauma can lead to a progressive neurodegeneration known as chronic traumatic encephalopathy. Although the medical literature also implicates head trauma as a risk factor for Alzheimer's disease, these findings are predominantly based on clinical diagnostic criteria that lack specificity. The dementia that follows head injuries or repetitive mild trauma may be caused by chronic traumatic encephalopathy, alone or in conjunction with other neurodegenerations (for example, Alzheimer's disease). Prospective longitudinal studies of head-injured individuals, with neuropathological verification, will not only improve understanding of head trauma as a risk factor for dementia but will also enhance treatment and prevention of a variety of neurodegenerative diseases.


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