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This paper highlights the importance of DNA damage as a contributory pathophysiological mechanism in ALS

Findings from the MTHFR heterozygous data-set have not been discussed in detail in this manuscript due to the fact that correlates within this data-set occupied an overlapping position between the other two data sets

PMID 28445289

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