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The human brain’s remarkably prolonged development is unique among mammals and is thought to contribute to our advanced learning abilities. Disruptions in this process may explain certain neurodevelopmental diseases.
Researchers at Queen’s University Belfast discovered how the journey or molecular pathway of an identified protein is both essential for brain development and how an alteration to its pathway could result in the spread of cancer.
The study, published today in Nature Cell Biology, has revealed the molecular mechanisms of a timely and spatially controlled movement of cells that is essential for the migration of newborn neurons during brain development and can also cause the spread of cancer, or cancer metastasis throughout the body.
It is expected this discovery will have a huge impact on the fundamental understanding of cancer metastasis and brain development and could lead to earlier diagnosis and better treatments, the research authors said.
Use of organophosphates has lessened, but risks to early brain development still too high. Public health experts have found there is sufficient evidence that prenatal exposure to widely used insecticides known as organophosphates puts children at risk for neurodevelopmental disorders.
In a scientific review and call to action published in PLOS Medicine, the researchers call for immediate government intervention to phase out all organophosphates...
(A) The location of area 10 of the prefrontal cortex (PFC) was determined using figures from Paxinos Stereotaxic Atlas (39). DAPI staining was used to differentiate the layers of the cortex, numbered 1–6. (B) Representative images of the differences seen in 5-HT fiber innervation of medial area 10 of the PFC between the four diet groups. (C) Exposure to a postweaning high-fat diet (HFD) decreased mean intensity of 5-HT immunoreactive signal in layer 1 of medial area 10 in the PFC (F1,16 = 7.662, p = 0.014). (D) 5-HT immunoreactivity in the same region was further affected by an interaction between gender and postweaning diet (F1,16 = 7.497, p = 0.015), with mean intensity decreased in postweaning HFD males compared to control males (F1,16 = 13.895, p = 0.002). Data shown as mean ± SEM...
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