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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.
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. J Neurosci.
2008 Jan 2;28(1):3-9.
PubMed Abstract
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Comment by: Lary Walker, ARF Advisor
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Submitted 7 January 2008
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Posted 7 January 2008
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The developing brain is particularly sensitive to environmental insults, including infection, radiation, and toxins. Because the brain is still growing, differentiating, and establishing connections at this time, such hazards can influence brain structure and function throughout the lifespan. For example, the risk of schizophrenia, a disorder that generally emerges in early adulthood, appears to be increased by specific maternal infections prenatally (Brown, 2006). Relatively little research has addressed the question of whether Alzheimer disease and other age-associated neurodegenerative disorders also might be promoted by brain changes incurred during development.
While the results involve a small number of animals and should be viewed as preliminary, the study of Wu and colleagues opens the door for further work in this area. These researchers studied the brains of eight female cynomolgus monkeys (Macaca fascicularis), four of which were exposed to low but biologically significant levels of lead acetate for the first 400 days of life. The animals showed no obvious...
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Comment by: Changiz Geula (Disclosure)
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Submitted 16 January 2008
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Posted 16 January 2008
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In this report, Wu et al. provide intriguing evidence that lead exposure during early postnatal life in female Macaca Fascicularis monkeys results in altered DNA methylation, oxidative stress, and changes related to amyloid pathology in late life. Expression of the genes for the amyloid precursor protein (APP) and its transcriptional regulator Sp1 was elevated in old animals that had been exposed to lead early during postnatal development. Significantly, these changes translated into elevated levels of the amyloid-β (Aβ) peptide, its intracellular accumulation, and increased deposition in cored plaques. These results replicate the author’s earlier findings in the rodent. These observations are provocative and enhance the possibility that early prenatal and/or postnatal events play a crucial role in initiation of disease. They invoke the probability that events in early life, including lead exposure, contribute to Alzheimer disease (AD) in late life. This line of research is worthy of pursuit in a larger cohort and as epidemiological study in humans.
Lary...
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Comment by: Gerta Farber
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Submitted 24 January 2008
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Posted 24 January 2008
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This new study indicates "evidence for a developmental origin and environmental link for Alzheimer's disease." The major unresolved question is the timing and the triggering leading to the disease, but data does suggest that a pathogenesis is influenced by early life exposures, with results not significant until later in life.
Genetic celiac disease has long been associated with neurologic and psychiatric disorders. Mayo Clinic has discovered a relationship of CD and dementia. When I was diagnosed with CD 6 years ago, at the age of 75, it was also revealed that in addition to my mother's autopsy in 1980 for AD, she possessed the gene responsible for my currently disabling CD.
I am aware that the past deaths of eight family members were attributed to "dementia," with the four most recent of those diagnosed as AD. My sibling has currently also been diagnosed with AD, as well as possessing a genetic celiac gene.
This new evidence of an environmental trigger to AD would warrant a study of gluten toxicity as a possible foundation.
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