The risk for developing the sporadic late-onset form of Alzheimer’s disease is attributable to an interaction of genetic and environmental factors. Among the genetic factors, it is well known that the presence of the APOE4 gene considerably increases the risk of developing the disease. Among environmental risk factors, lifestyle measures (such as diet, sleep quality, physical activity, and mental training) and exposure to toxic agents have great importance for prevention, since they can be modified both at the individual level and through collective health policies. Despite its relevance, the effect of exposure to toxins has not been properly studied: the number of articles published on this subject is limited, and occur mostly in journals on environment and toxins rather than in medical journals.
Within environmental toxins, pesticides represent a major threat because they can remain in the environment for a long time (years or decades) and also because they accumulate in the tissues of animals and humans – they are therefore classified as Persistent Organic Pollutants (POPs). POPs persist in the environment, accumulate through food chains, and pose a major risk to the environment and human health.
Some epidemiological studies show a clear association of occupational exposure to pesticides and the development of Alzheimer’s disease, especially in people who work in the field applying the product directly to the soil. However, it has been shown that even individuals who do not work exposed to pesticides, nor live in areas of high risk of contamination, have high levels of pesticides or their metabolites in their blood. In 2009  a small study showed that serum levels of DDE (p,p’-dichlorodiphenyldichloroethylene), a metabolite of the organochlorine pesticide DDT (dichlorodiphenyltrichloroethane), were higher in Alzheimer patients compared to control group participants.
In 2014, a study that further evaluated the association of the pesticide DDT with Alzheimer’s disease was published in The Lancet Neurology journal  and deserves to be described in detail due to the importance of its findings. The study carried out different experiments, aiming to confirm that association. First, the presence of the metabolite DDE in the blood of Alzheimer patients and in control group was evaluated, in a larger group than the study published in 2009. The APOE genotype (determination of the patient’s APOE type) was also performed in order to correlate genetic variable to pesticide exposure.
In parallel, brains of individuals diagnosed with Alzheimer’s were studied (post-mortem), measuring the amount of the pesticide in brain tissue and correlating these values with values of the DDE measurement in blood collected before the patient’s death.
Finally, an in vitro experiment was conducted where brain cells were exposed to DDE/DDT in order to assess the production of APP – the precursor protein of amyloid Beta – in response to the presence of the pesticide. Amyloid Beta is the component of the deposits (plaques) characteristic of Alzheimer’s disease.
And what were the results of this study?
- Although the presence of DDE was detected in both control group and Alzheimer cases (which confirms that this pesticide is present in almost the entire population, regardless of occupational exposure), the concentration of this metabolite was significantly higher in patients than in controls. Also, the higher the concentration in the blood, the greater the cognitive deficit (as measured by the Mini Mental State Examination -MMSE). This confirms that the presence of DDE/DDT in the blood is associated with both the development of Alzheimer’s and the severity of the disease, i.e., the higher the blood level of DDE, the more severe are the symptoms.
- DDE was detected in brain tissue of patients diagnosed with Alzheimer’s disease and the brain levels showed a good correlation with the levels detected in the blood, indicating that this toxin easily crosses the blood-brain barrier.
- The presence of APOE 4 associated with high blood levels of DDE resulted in an even higher risk for cognitive impairment, confirming that overlapping risk factors contribute to an additive effect regarding the risk of disease development and severity of symptoms.
- Exposure of human brain cells to DDE/DDT increased the production of amyloide precursor protein (APP), evidencing that this toxin can induce the formation of amyloid plaques – a major pathological marker of Alzheimer’s disease.
Taken together, these findings identify DDT (and its metabolite DDE) as an important environmental risk factor for Alzheimer’s disease.
DDT (dichlorodiphenyltrichloroethane) was extensively used between the 1940s and 1970s around the world both in agriculture and as an insecticide to control vector-borne diseases, including malaria. As it showed no short-term harm in humans, this product continued to be used and for some time was recognized as a great scientific discovery. However, after 20 years of indiscriminate use, its effects in nature – including the death of birds and fish – and on human’s health (association with cancer cases and proved hormonal disbalance effect), led to the banning of this substance in 1972 in the United States and Europe. However, DDT continues to be used legally and illegally in developing countries. Although controversial, the World Health Organization supported reintroduction of DDT for malaria eradication in 2006 . Thus, there is still significant exposure of human population.
Despite the frightening results, there are few studies investigating the neurotoxic potential of DDE/DDT. It is also clear that controlling insect-borne infectious diseases is a serious problem in developing countries and that it is important to secure crops (even at a high price) in regions where hunger still exists. However, with the knowledge and technology of today’s world, it should be possible to find ways and solutions that are less harmful to the health of the planet and people.
DDT is a pesticide that was widely used between 1940 and 1970 in agriculture for crop protection and additionally as an insecticide for infection prevention, but is still used today in developing countries. However, this substance is degraded very slowly and therefore accumulates both in the environment and in living organisms. In addition to its proven carcinogenic and hormone-disrupting effects, recent studies show a link between this toxin and the development of Alzheimer’s disease. A 2014 study showed that Alzheimer’s patients have higher levels of DDT in their blood than normal people and that this toxin (and its metabolite DDE) is able to cross the blood-brain barrier and contaminate the brain. Thus, exposure to DDT is an environmental risk factor for the development of Alzheimer’s disease and should be avoided at both the individual and public health levels.
Therefore, make use of this knowledge and continue to inform yourself at the project “Knowledge stops dementia” how you can protect yourself and your brain health despite this risk factor. Thus, you can act individually to prevent Alzheimer’s disease and also have the competence to advocate for a meaningful community health policy!
- ↑ Richardson JR, Shalat SL, Buckley B, Winnik B, O’Suilleabhain P, Diaz-Arrastia R, Reisch J, German DC. Elevated serum pesticide levels and risk of Parkinson disease. Arch Neurol. 2009 Jul;66(7):870-5. doi: 10.1001/archneurol.2009.89. PMID: 19597089; PMCID: PMC3383784.
- ↑ Richardson JR, Roy A, Shalat SL, von Stein RT, Hossain MM, Buckley B, Gearing M, Levey AI, German DC. Elevated serum pesticide levels and risk for Alzheimer disease. JAMA Neurol. 2014 Mar;71(3):284-90. doi: 10.1001/jamaneurol.2013.6030. PMID: 24473795; PMCID: PMC4132934.
- ↑ Rehwagen C. WHO recommends DDT to control malaria. BMJ. 2006 Sep 23;333(7569):622. doi: 10.1136/bmj.333.7569.622-b. PMID: 16990319; PMCID: PMC1570869.
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