Early exposure to lead causes Alzheimers pathology

[Kathy]

As I have said, the timing of exposure to toxic metals, eg here - Lead, results in a different outcome than "adult" exposure.

These monkeys show changes in their protein expression, and resulting amyloid plaques as seen in Alzheimer's disease, as a result of exposure to lead in formula during the first 400 days post weaning.

J Neurosci. 2008 Jan 2;28(1):3-9.

Alzheimer's disease (AD)-like pathology in aged monkeys after infantile exposure to environmental metal lead (Pb): evidence for a developmental origin and environmental link for AD.

Wu J, Basha MR, Brock B, Cox DP, Cardozo-Pelaez F, McPherson CA, Harry J, Rice DC, Maloney B, Chen D, Lahiri DK, Zawia NH.
Department of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston, Rhode Island 02881, USA.

The sporadic nature of Alzheimer's disease (AD) argues for an environmental link that may drive AD pathogenesis; however, the triggering factors and the period of their action are unknown. Recent studies in rodents have shown that exposure to lead (Pb) during brain development predetermined the expression and regulation of the amyloid precursor protein (APP) and its amyloidogenic beta-amyloid (Abeta) product in old age. Here, we report that the expression of AD-related genes [APP, BACE1 (beta-site APP cleaving enzyme 1)] as well as their transcriptional regulator (Sp1) were elevated in aged (23-year-old) monkeys exposed to Pb as infants. Furthermore, developmental exposure to Pb altered the levels, characteristics, and intracellular distribution of Abeta staining and amyloid plaques in the frontal association cortex. These latent effects were accompanied by a decrease in DNA methyltransferase activity and higher levels of oxidative damage to DNA, indicating that epigenetic imprinting in early life influenced the expression of AD-related genes and promoted DNA damage and pathogenesis. These data suggest that AD pathogenesis is influenced by early life exposures and argue for both an environmental trigger and a developmental origin of AD.

PMID: 18171917

essential information for doing more truthful studies on cattle and exposure to the various environmental toxins out there, aka: lead, uranium, cesium, strontium, barium, tungsten, molybdenum......

The effects on developing fetus, infant and children (when cells are multiplying and dividing quickly), is more profound than the effects on a fully developed adult.

Lead levels remain higher in the brain in exposed monkeys than controls, even though blood levels balance off after lead exposure over time.

 

[MoGal]

Do you know if they did any studies giving them EDTA to reverse the lead?

I think that's one of the reasons they are testing preschool and school age children for metals as they are having a much higher percentage in their system and I'm not sure if or how much EDTA children can take.