Abstract Details

Title Preliminary neuropathological findings in porcine brains following hypobaric exposure

Topic Aging, Dementia, and Behavioral Neurology

Presentation(s) P5 - Poster Session 5 (5:30 PM-6:30 PM)

Poster/Presentation
Number 1-004

Objective Determine neuropathological effects of repeated hypobaric exposure on the brain in an animal/swine model

Background Repeated human exposure to extreme hypobaria (low atmospheric pressure) is associated with increased white matter hyperintensities (WMH) in humans as observed on T2-weighted imaging and decline of axonal integrity as measured by fractional anisotropy in both humans and swine (sus scrofa) animal models. While WMH’s were not observed in the swine model, we hypothesize that neuropathological analysis of the porcine brains coupled with MRI analysis will shed light on the underlying pathophysiological process in both humans and animals exposed to hypobaric environments.

Design/Methods Brains from four adolescent age porcine (sus scrofa) animals exposed to 30k feet chamber flights on 100% FiO2, each lasting eight hours, occurring every three days for total of six flights were examined and contrasted to four porcine “control” brains who were exposed to six sham flights without hypobaric exposure. Samples were sent to the Center of Neuroregenerative Medicine and pathology specimens were reviewed by a blinded neuropathologist skilled in animal neuropathology.

Results

Preliminary results demonstrate immunoreactivity to AT8 (hyper-phosphorylated tau protein) TAU-pathology, along with TAU-tangles to pre-tangles in cortical layer 3 of the temporal cortex and hippocampus in two of four exposed and control animals. Staining for amyloid precursor protein, glial fibrillary astrocytic protein (marker for inflammation), and myelin basic protein (marker for demyelination) were negative.

Conclusions The incidence of TAU-pathology in the form of both tangles, pre-tangles and hyper-phosphyorylated tau has not been reported in swine models before. The presence of TAU-pathology in both exposed and control adolescent groups is unclear in the absence of demyelination or inflammatory changes, although the “n” is small (8). Further sampling and analysis (already underway) is required. However, such findings are instrumental to elucidate the underlying pathophysiology of hypobaric effects on the brain leading to optimal mitigation strategies.

Authors/Disclosures
Melissa Cook, MD PRESENTER	Dr. Cook has nothing to disclose.
	No disclosure on file
John H. Sladky, MD, FAAN (San Antonio Military Medical Center/MCHE MDU)	Dr. Sladky has nothing to disclose.

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