Abstract
ObjectiveThis study sought to determine if there is an association between variants in the apolipoprotein E (ApoE) promoter regions and development of white matter hyperintensities (WMH) in military subjects who have been exposed to high altitude. In an earlier study, we found that ApoE status did not correlate with WMH development, and here we hypothesized that regulation of APOE protein expression may be protective.ResultsOur cohort of 92 subjects encountered altitude exposures above 25,000 feet mean sea level through their occupations as pilots or altitude chamber technicians. Using Taqman-style polymerase chain reaction genotyping and t-tests and two-way analyses of variance we found no significant association between ApoE promoter genotypes and the presence, volume, or quantity of WMHs after high altitude exposure. Taken together, the observations that neither ApoE genotype status nor promoter status are associated with WMH properties, we believe that the mechanism of action for developing WMH does not derive from ApoE, nor would therapies for ApoE-mediated neurodegeneration likely benefit high altitude operators.
Highlights
White matter hyperintensities (WMH) are small lesions in the brain that appear as bright signals on an magnetic resonance imaging (MRI) radiograms [1]
ApoE2 status correlates with increasing brain WMHs [11], and apolipoprotein E (ApoE) genotype status is associated with traumatic brain injury recovery [10] as well as risk of hemorrhagic and ischemic cerebrovascular disease [11]
As more high performance aircraft are being developed with service ceilings greater than 50,000 feet, and as commercial space flight is a reality, there is a clear need to understand the impacts of flight on physiology and to identify how an individual may be more resilient or susceptible to these impacts
Summary
White matter hyperintensities (WMH) are small lesions in the brain that appear as bright signals on an MRI (magnetic resonance imaging) radiograms [1]. These lesions have been associated with decreased cognitive performance [2] and decreased cerebral blood flow [3]. For those rare populations that encounter extreme high altitudes (greater than 25,000 feet above mean sea level), there is a real risk of repetitive non-hypoxic hypobaria resulting in neurological defects. ApoE4 is associated with an increased risk of Alzheimer’s disease [12, 13], and yet is protective in people who consume high levels of fish [14]. We did not find a significant association between ApoE genotype status and altitude-associated WMH [7]
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