By NASA/JPL-Caltech/SwRI - http://photojournal.jpl.nasa.gov/jpeg/PIA16938.jpg, Public Domain, https://commons.wikimedia.org/w/index.php?curid=26429266
Galactic cosmic radiation may prove a problem for deep-space travel, and a study demonstrates that similar high-intensity radiation in mice caused cognitive decline and changes in gene expression in the hippocampus (a part of the brain whose importance is discussed in the abstract reproduced below). One wonders if long exposure to the less intense, lower energy cosmic radiation that we are exposed to on the Earth's surface contributes to cognitive decline with age. Therefore, the hypothesis is that long-term exposure to weaker cosmic radiation may have similar effects to short-term exposure to more intense cosmic radiation. On the other hand, it may be possible there is a threshold effect and only high energy does the damage. We may be adapted to deal with lower level radiation on the Earth's surface; however, cognitive decline with old age may not be strongly selected against if it is far enough removed from the reproductive age. In summary it is a hypothesis worth looking into. Abstract:
Radiation from galactic cosmic rays (GCR) poses a significant health risk for deep-space flight crews. GCR are unique in their extremely high-energy particles. With current spacecraft shielding technology, some of the predominant particles astronauts would be exposed to are 1H + 16O. Radiation has been shown to cause cognitive deficits in mice. The hippocampus plays a key role in memory and cognitive tasks; it receives information from the cortex, undergoes dendritic-dependent processing and then relays information back to the cortex. In this study, we investigated the effects of combined 1H + 16O irradiation on cognition and dendritic structures in the hippocampus of adult male mice three months postirradiation. Six-month-old male C57BL/6 mice were irradiated first with 1H (0.5 Gy, 150 MeV/n) and 1 h later with 16O (0.1 Gy, 600 MeV/n) at the NASA Space Radiation Laboratory (Upton, NY). Three months after irradiation, animals were tested for hippocampus-dependent cognitive performance using the Y-maze. Upon sacrifice, molecular and morphological assessments were performed on hippocampal tissues. During Y-maze testing, the irradiated mice failed to distinguish the novel arm, spending approximately the same amount of time in all three arms during the retention trial relative to sham-treated controls. Irradiated animals also showed changes in expression of glutamate receptor subunits and synaptic density-associated proteins. 1H + 16O radiation compromised dendritic morphology in the cornu ammonis 1 and dentate gyrus within the hippocampus. These data indicate cognitive injuries due to 1H + 16O at three months postirradiation.
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