28 January 2014. The increasing occurrence of Alzheimer’s disease cannot be explained by genetic inheritance only. There must be some environmental factors involved. Thus, head trauma is a risk factor that has been supported by robust scientific documentation. Yesterday, a group of US neurologists published a report on the concentrations of the pesticide DDT and its DDE metabolite in serum from Alzheimer patients and comparable healthy controls. Using serum samples collected between 2002 and 2008, they found average concentrations that were 3.8-fold higher in the Alzheimer cases, as compared with the control participants. This difference is statistically highly significant.
Still, some of the serum samples contained pesticide concentrations below the detection limit – 30% of controls and 20% of cases had unmeasurable DDE levels. Thus, the difference between the two groups was driven by the Alzheimer patients with high pesticide levels in the serum. An increased risk was apparent only among subjects whose concentration was in the top third. The results are in accordance with DDT being a chemical brain drainer.
This new evidence does not negate the importance of genetic risks. About 20 genes are known to be associated with increased risk for late-onset Alzheimer’s disease, but most has only a small effect on risk. Only the Apolipoprotein E (APOE) gene is a common and potent risk factor – each mutation of the gene increases the risk by 3-fold. This tendency was also apparent in the new study released yesterday. The new study showed that DDT exposure together with APOE mutations increased the risk of Alzheimer even further.
Experimental studies suggest that exposure to chemical brain drainers, such as lead, can affect gene expression and the production of certain proteins that are associated with Alzheimer’s disease. Adults who had a high lead concentration in their umbilical cord blood at birth showed biochemical changes related to the generation of amyloid proteins typical of Alzheimer’s disease.
As another example, a recent study in Korea showed that the presence of APOE mutations exacerbated the adverse effects of methylmercury on children’s neurodevelopment at age 2. So this important genetic risk factor for Alzheimer may already be operating during brain development. Will mercury-exposed subjects have less reserve capacity to withstand the disease? We don’t know, but a hypothesis that Alzheimer’s disease may be triggered by environmental chemicals is certainly plausible.
Still, skull trauma remains the only certain risk factor. Is this because physical injury is much more important than chemical damage? Probably not. Information on skull trauma can be easily obtained from the past medical history and hospital charts. In contrast, the information available on early-life or other past exposures to neurotoxic chemicals is almost non-existent. The new study took advantage of the fact that DDT – and especially its break-down product DDE – is highly persistent and will remain in the body for many years after the exposure. The researchers even showed that brain tissue from autopsies contained DDE at levels that were proportional to those that occurred in the blood. Thus, a recent serum sample, even if taken at the time of diagnosis, could reveal information on exposures that occurred in the past. However, whether serum concentrations in adults also reflect their early-life exposures is questionable.
Laboratory models suggest that some industrial pollutants can elicit biochemical effects related to Alzheimer’s disease. So skull trauma is definitely not the only environmental risk factor. Yet, we don’t know what those other factors are. The evidence is not available to draw a conclusion, but substances that are toxic to the brain must be regarded highly suspect in this regard.