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have indicated the Al has no effect. [48-50] The same can be exacerbate oxidative stress. Thus, the aim of this study
said for lead (Pb), mercury (Hg), methylmercury (MeHg), was to determine the impact of environmental toxins
iron (Fe), zinc (Zn), etc. [51-54] The association between on the pathogenesis of AD. The overall hypothesis
solvent exposure and AD is weak and in some cases is that environmental influence occurring during
contradictory. [55,56] In addition, electromagnetic fields brain development and beyond result in damage to
have a tenuous relationship to AD. [57,58] Finally, various mitochondria, and reprogramming of the brain resulting
pesticides have been linked to AD as well as other in increased oxidative stress and inflammation. [62,63] This
neurological disorders especially Parkinson’s disease. process alters expression of various genes related to the
The effects of specific pesticides (organophosphates development of AD (increased APP expression, increase
and carbamates) on the brain are well known and APP processing), which further exacerbates the disease
contribute to a number of pathological features. Tyas course. [64] This susceptibility early in life exacerbates
et al. [38] and Baldi et al. [40] showed that occupational the normal process of amyloidogenesis in the aging
exposure to defoliants/fumigants or general brain, accelerating the onset of AD. [65] Several studies
pesticides as statistically limited to AD. Furthermore, have suggested in human studies or demonstrated in
epidemiological studies have demonstrated that specific animal studies that environmental toxins do influence
organochlorides (dichlorodiphenyltrichloroethane, neurodegeneration and neurobehavioral function. [44,65-68]
dichlorodiphenyldichloroethylene and dieldrin) Stewart et al. [67] showed that APOE genotype and
were present in the brains of both AD and Parkinson’s previous exposure to lead can alter behavioral aspects of
disease patients suggesting an etiological relationship aged individuals. In addition, they showed that magnetic
for these chemicals. [59] resonance imaging analysis of these individuals showed
increased neurodegeneration compared to individuals
The findings of this study address the impact of not exposed to lead. [66] Finally, Zawia has shown that
environmental factors on the which exacerbates exposure of rats and mice to lead early in life can
brain biochemical processes and memory deficits exacerbate APP processing and amyloid formation in
upon exposure in a mouse model expressing the APP the brain. [44,65,68]
transgene that is relevant to sporadic AD patients,
representing more than 90% of the AD population. In conclusion, this study shows that exposure of APP
Environmental factors have been viewed in the field as transgenic mice to pesticides as different times during
potential targets for therapeutic intervention to prevent development results in enhanced memory deficits and
or attenuate pathology and memory deficits associated altered brain APP metabolism. In addition, we show
with AD. [44] Identification of such pathways involved that the CPO exacerbates inflammation, oxidative stress
in enhanced memory deficits was accomplished in this and suppresses neurotrophic factor expression that
study by using the APP mouse model of AD. [28] may contribute to the disease process. Importantly,
these data validate the impact of environmental toxins
Treatment of mice in utero, during neonatal development on the enhancement of AD pathology and suggest that
or as adults resulted in an altered biomarker pattern this process may contribute to the development and
consistent with enhanced AD-like activity. Biomarker progression of AD in people.
analyses showed that pesticide exposure of the APP
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40 Neuroimmunol Neuroinflammation | Volume 2 | Issue 1 | January 15, 2015