Fluoride is a potential cause of Alzheimer’s

This new study1 suggests that most cases of Alzheimer’s Disease can be attributed to environmental factors and that fluoride is a potential cause because it easily crosses the blood–brain barrier.

The research presented in this review clearly indicates that fluoride may play a key role in the induction and development of inflammation in Alheimer's disease and participate in processes of neurodegeneration.

Marta Goschorska, lead author
Abstract

The etiopathogenesis (cause and subsequent development) of Alzheimer’s disease (AD) has not been fully explained. Now, the disease is widely attributed both to genetic and environmental factors. It is believed that only a small percentage of new AD cases result solely from genetic mutations, with most cases attributed to environmental factors or to the interaction of environmental factors with preexistent genetic determinants. Fluoride is widespread in the environment and it easily crosses the blood–brain barrier. In the brain fluoride affects cellular energy metabolism, synthesis of inflammatory factors, neurotransmitter metabolism, microglial activation, and the expression of proteins involved in neuronal maturation.

Fluoride as a Neurotoxic Agent

Fluoride is widespread in the environment, especially in industrial areas. It easily crosses the blood–brain barrier, wherein the accumulation of fluoride disturbs phospholipid metabolism leading to neuronal death. In overexposed women, fluoride can also pass through the blood–placenta barrier to enter the fetal circulation, where it has been shown to inhibit central nervous system development and cause neurodegeneration. In recent years, the mechanism and extent of fluoride’s effect on the nervous system have been the subject of increasing scientific interest.

The effect of fluoride exposure on the developing brain (both pre- and neonatal) manifests clinically as memory loss and impairment of cognitive processes. Epidemiological studies showed that children living in areas with excessive fluoride exposure had lower IQ values compared to less exposed children.

Fluoride-induced abnormalities are associated with disturbed metabolism of neurons and glial cells. Fluoride accumulation in the hippocampus has been found to contribute to neuronal degeneration and altered oxygen metabolism, promoting the formation of ROS, and inducing damaging oxidative stress.

More recent studies have shown that the effect of fluoride on the central nervous system may be extremely varied and complex. In addition to its pro-oxidative effect, fluoride has demonstrated an influence on the activity of antioxidative enzymes, further encouraging damaging levels or ROS. Fluoride has also been found to affect cellular energy metabolism, synthesis of inflammatory factors, neurotransmitter metabolism, microglial activation, and the expression of proteins involved in neuronal maturation. Finally, and of specific importance to its role in Alzheimer’s disease, studies report fluoride-induced apoptosis and inflammation within the central nervous system.

Conclusions

Alzheimer’s disease is one of the most common causes of dementia. Its clinical presentation, including memory impairment, cognitive disorders, and neuropsychiatric symptoms, results from pathomorphological and pathophysiological changes in the central nervous system.

The research presented in this review clearly indicates that fluoride may play a key role in the induction and development of inflammation in AD and participate in processes of neurodegeneration. Fluoride may promote the synthesis of proinflammatory factors (e.g., prostaglandins and proinflammatory cytokines including IL6, TNF-α, IL1B, IL-4, and IFN-γ), transcription factors (c-Jun and NF-κB), and proapoptotic proteins (Bax, p53, and FAS receptor protein), as well as reduce synthesis of antiapoptotic proteins (BCl-2 and BCLXL).

Moreover, fluoride has been shown to affect the expression and activity of enzymes involved in inflammation (e.g., COX-2) and alter oxidative balance (i.e., modify ROS levels, cause dysfunction in activity and expression of SOD, CAT, GPx, GR, and GSH).

In summary, the influence of fluoride on processes of AD initiation and progression is complex, not yet fully understood, and warrants further investigation, especially considering growing environmental fluoride pollution.

  1. Goschorska M, et al, “Potential Role of Fluoride in the Etiopathogenesis of Alzheimer’s Disease,” International Journal of Molecular Science; 2018 Dec; 19(12): 3965. Full study available here.