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Environmental mold exposure, brain inflammation, and spatial memory deficits

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Abstract

Approximately 40% of American buildings are moldy. Early studies found that neurologists could not differentiate between people who lived or worked in moldy buildings and patients with mild to moderate traumatic brain injury—they had the same neurological and cognitive deficits. Our laboratory developed a mouse model to determine how mold exposure might lead to cognitive dysfunction. One critical issue is whether exposure to any mold causes problems or only exposure to extremely toxic molds like Stachybotrys. We therefore quantified the effects of exposure to (1) intact Stachybotrys spores (IN) containing a variety of toxins, volatile organic compounds and proteinases, (2) Stachybotrys spores extracted twice with ethanol (EX) to remove toxins and denature proteins, or (3) the nonpyrogenic saline vehicle (VEH). Mice were nasally instilled 3X per week. After 5 weeks, EX mice performed significantly worse in finding the hidden platform in the Morris water maze (MWM) than VEH or IN mice, taking longer to find the platform and using longer paths. Surprisingly. IN mice showed evidence of lesser memory impairment. MWM performance in EX and IN mice was inversely correlated with numbers of interleukin-1β cells in dorsomedial CA1 as well as with weight gain over the first 3 weeks of treatment. Clearly, exposure to just the mold skeleton is sufficient to cause brain inflammation and cognitive deficits, suggesting exposure to any mold could be problematic.

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... In human, truncal, but not selective, vagotomy may protect against PD development (31). Harding et al (32) found that nasal exposure of spores of the common stachybotrys (black toxic) mold induced brain inflammation and spatial memory deficit in mice. Furthermore, also in mice but using fibrils of either human or mouse α-syn, Rey et al. (33) provided the first evidence of a transneuronal, progressive propagation of PDlike α-syn pathology from the olfactory bulb to central brain regions. ...
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The authors support the hypothesis that a causative agent in Parkinson's disease (PD) might be either fungus or bacteria with fungus-like properties – Actinobacteria, and that their spores may serve as ‘infectious agents’. Updated research and the epidemiology of PD suggest that the disease might be induced by environmental factor(s), possibly with genetic susceptibility, and that α-synuclein probably should be regarded as part of the body's own defense mechanism. To explain the dual-hit theory with stage 1 involvement of the olfactory structures and the ‘gut-brain’-axis, the environmental factor is probably airborne and quite ‘robust’ entering the body via the nose/mouth, then to be swallowed reaching the enteric nervous system with retained pathogenicity. Similar to the essence of smoking food, which is to eradicate microorganisms, a viable agent may be defused by tobacco smoke. Hence, the agent is likely to be a ‘living’ and not an inert agent. Furthermore, and accordant with the age-dependent incidence of LPD, this implies that a dormant viable agent have been escorted by α-synuclein via retrograde axonal transport from the nose and/or GI tract to hibernate in the associated cerebral nuclei. In the brain, PD spreads like a low-grade infection, and that patients develop symptoms in later life, indicate a relatively long incubation time. Importantly, Actinomyces species may form endospores, the hardiest known form of life on Earth. The authors hypothesize that certain spores may not be subject to degradation by macroautophagy, and that these spores become reactivated due to the age-dependent or genetic reduced macroautophagic function. Hence, the hibernating spore hypothesis explains both early-onset and late-onset PD. Evaluation of updated available information are all consistent with the hypothesis that PD may be induced by spores from fungi or Actinobacteria and thus supports Broxmeyer’s hypothesis put forward 15 years ago.
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