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It is expected that polymorphisms in NER or BER genes may modulate individual susceptibility to PAHs exposure.
An alternative interpretation of our results is that, given the lack of association with Aβ42 and ptau181, variants in these genes may modulate risk for AD through mechanisms that do not directly alter CSF levels of Aβ42 or ptau181.
These results suggest that genetic variations among inflammation pathway genes may modulate the development of radiation-induced toxicity and, ultimately, help in identifying patients who are at an increased likelihood for such events.
Future studies will be directed at determining whether and/or how these genes may modulate different aspects of song production and/or learning, the main functions of song nucleus HVC.
Such genes may modulate the expression of resistance genes in response to the pathogen infection.
Thus, variants in detoxification genes may modulate the effects of in utero exposure through epigenetic mechanisms.
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Because glutathione S-transferases (GSTs) are the major detoxification enzymes which protect cells against oxidative stress, genetic variations in the GST gene may modulate the risk of POP.
We hypothesize that alternative splicing of the 5′UTRs of this gene may modulate differential expression patterns.
Thus, genetic variation in the DTNBP1 gene may modulate schizophrenia susceptibility by altering DTNBP1 expression in areas of the brain crucial for cognitive functions.
The g.3296G>A, g.3481A>G, c.–2G>A and polymorphisms of the TF gene may modulate the risk of keratoconus, by its involvement in altered iron homoeostasis and oxidative stress induction.
As a result of this association of the polymorphic allele with distribution of body fat storage, we suggest that genetic variability in the ADIPOQ gene may modulate the levels of sAdiponectin.
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