Environmental risk factors provoke new thinking for prevention and treatment of dementia with Lewy bodies

Abstract

In recent years, environmental factors have received attention in the pathogenesis of neurodegenerative diseases. Other than genetic factors, the identification of environmental factors and modifiable risk factors may create opportunities to delay the onset or slow the progression of Lewy body disease. Researchers have made significant progress in understanding environmental and modifiable risk factors over the past 30 years. To date, despite the increasing number of articles assessing risk factors for Lewy body disease, few reviews have focused on their role in its onset. In this review, we reviewed the literature investigating the relationship between Lewy body disease and several environmental and other modifiable factors. We found that some air pollutants, exposure to some metals, and infection with some microorganisms may increase the risk of Lewy body disease. Coffee intake and the Mediterranean diet are protective factors. However, it is puzzling that low educational levels and smoking may have some protective effects. In addition, we proposed specific protocols for subsequent research directions on risk factors for neurodegenerative diseases and improved methods. By conducting additional case-control studies, we could explore the role of these factors in the etiopathogenesis of Lewy body disease, establishing a foundation for strategies aimed at preventing and reducing the onset and burden of the disease.

Highlights

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  Coffee intake and the Mediterranean diet are low risk factors associated with Lewy body dementia.

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  Infection with some pathogenic organisms may be associated with an increased risk of Lewy body dementia.

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  Low educational level and heavy smoking may have some protective effect in Lewy body dementia.

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  Air pollution exposure may act as trigger factor in Lewy body dementia.

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  Some heavy metals may be significantly relevant to the onset of Lewy body dementia by increase the aggregation of a-synuclein.