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Furthermore, auranofin treatment increases SORLA levels and reduces A levels in human AD neurons in a SORLA-dependent manner, further supporting the blockade of PKC/ as an effective strategy to increase SORLA levels and mitigate AD pathogenesis

doi: 10.1111/j.1749-6632.2009.04754.x

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Hendriks et al [3] preferred Pronase because of the uncertain commercial availability of the enterotoxin and the latters possible cause of cell blebs

Research has shown that mycotoxins can disrupt several cognitive processes by: Impairing mitochondrial function in neurons, reducing energy available for brain cells Disrupting the production and regulation of key neurotransmitters Causing oxidative stress that damages neural tissue Affecting myelination, which impacts the speed and efficiency of neural transmission Disrupting neurogenesis (the creation of new brain cells) in the hippocampus, a region vital for learning and memory These mechanisms help explain the constellation of cognitive symptoms frequently reported with mold exposure: Difficulty with word-finding and verbal fluency Problems with short-term memory and information retention Challenges with executive function, planning, and organization Reduced processing speed and mental clarity Difficulty with math and spatial reasoning Recognizing the Signs of Mold-Related Brain Effects One of the most challenging aspects of mold-related brain symptoms is that they often fluctuate and may seem disconnected from any obvious environmental cause