2022
DOI: 10.1016/j.tox.2022.153358
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β-N-Methyl-Amino-L-Alanine cyanotoxin promotes modification of undifferentiated cells population and disrupts the inflammatory status in primary cultures of neural stem cells

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Cited by 3 publications
(4 citation statements)
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“…The most robust upregulation was seen in IL-6, which expression has been shown to be related to hyposmia, inversely correlated with cognitive test scores, and proceeds the development of senile plaques, a hallmark of AD [72] , [73] , [74] . These findings suggest that chronic BMAA exposure to olfactory tissues may increase gene expression profiles that can cause neuroinflammation and olfactory dysfunction in susceptible individuals [75] , [76] .…”
Section: Discussionmentioning
confidence: 81%
“…The most robust upregulation was seen in IL-6, which expression has been shown to be related to hyposmia, inversely correlated with cognitive test scores, and proceeds the development of senile plaques, a hallmark of AD [72] , [73] , [74] . These findings suggest that chronic BMAA exposure to olfactory tissues may increase gene expression profiles that can cause neuroinflammation and olfactory dysfunction in susceptible individuals [75] , [76] .…”
Section: Discussionmentioning
confidence: 81%
“…We thus aimed at determining the effects of marennine on immunocompetent cell populations and activation. The activation status of these immunocompetent cells is referred to as the balance ratio between CD86 + and CD206 + [ 48 , 49 ]. Whatever marennine concentration, no harmful effect could be observed after 24 h of exposure, neither on astrocytes nor microglial cell population, at 10 or 50 µg/mL.…”
Section: Discussionmentioning
confidence: 99%
“…Perinatal exposure in mice, even with low doses of BMAA, leads to neurobehavioral disturbances during the postnatal period and adulthood [ 302 ]. Moreover, BMAA modifies neuroblast organization increasing the number of neuroblasts clusters [ 303 ].…”
Section: Mechanisms Of Brain Toxicitymentioning
confidence: 99%
“…Both glial cells and neurons can uptake and accumulate BMAA, as demonstrated using a specific polyclonal antibody against BMAA [ 333 ]. BMAA induces a proinflammatory response in astrocytes and microglial cells, causing a shift in the ratio of CD86/CD206 cells [ 303 , 334 ].…”
Section: Mechanisms Of Brain Toxicitymentioning
confidence: 99%