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1g), but only significantly downregulated the hypoxia-induced increase in secretion of d-serine, not l-serine (Fig

Hwang S, Mruk K, Rahighi S, Raub AG, Chen CH, Dorn LE, et al

Studies from this group support that Pb can disrupt the brain export of A leading to its accumulation and plaques formation (Behl et al., Exposure to Pb during development is a good example of an environmental contaminant as a risk factor to promote neurodegenerative diseases such as AD, supporting the hypothesis that many adult diseases have a fetal origin (FeBAD) (Basha et al., APP mRNA expression as well as in the activity of the transcription factor Sp1 (one of the regulators of APP ) in the cortex of neonates, and after 20 months of Pb exposure had ceased

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The Nrf2 pathway operates via a Keap1-mediated mechanism where oxidative stress triggers Nrf2 release, allowing its nuclear translocation and binding to antioxidant response elements (Shen et al., 2019)