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Particulate Matter and Alzheimer's Disease - An Intimate Connection - ScienceDirect
Particulate Matter and Alzheimer's Disease - An Intimate Connection - ScienceDirect
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https://doi.org/10.1016/j.molmed.2022.06.004
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The environmental role in disease progression has been appreciated for decades; however, understanding
how airborne toxicant exposure can affect organs beyond the lungs is an underappreciated area of scientific
inquiry. Particulate matter (PM) includes various gases, liquids, and particles in suspension and is produced
by industrial activities such as fossil fuel combustion and natural events including wildfires and volcanic
eruptions. Although agencies have attempted to reduce acceptable airborne particulate levels, with
urbanization and population growth, these policies have been only moderately effective in mitigating
disease progression. A growing area of research is focused on the role of PM exposure in the progression of
Alzheimer’s disease (AD). This review will summarize the knowns and unknowns of this expanding field.
Section snippets
PM consists of a heterogeneous mixture of solid and liquid particles suspended in the air (Box 1) [1]. Current
research has established compelling relationships between PM exposure and the development of ischemic
heart disease, myocardial infarction, and lung diseases, including aggravated asthma [1,2]. These connections
are alarming due to the significant number of individuals routinely exposed to dangerous PM levels
worldwide. Importantly, recent studies have also established connections…
Concluding remarks
Understanding how the environment can affect health and disease progression is important to inform policy
as well as design novel mitigation strategies to combat the increase in PM-associated illness. It is apparent
that exposure to consistently high levels of PM can have significant effects on AD progression; however,
additional studies are needed to understand the mechanisms whereby PM exposure affects the brain and
associated organs. Additionally, the majority of studies on PM-induced AD…
Acknowledgments
This work was supported by salary support for Dr Yael-Natalie H. Escobar (T32HL149637) and grants from
the National Institutes of Health (R01 HL139348, R01 AG057046) and the American Heart Association
(20YVNR35490079) to L.E.W. All figures were created using BioRender.com .…
Declaration of interests
Glossary
Aβ40
40-residue peptide derived from the cleavage of the protein amyloid precursor protein; it is a major
component of Aβ plaques.
Aβ42
42-residue peptide derived from the cleavage of the protein amyloid precursor protein; it is a major
component of Aβ plaques.
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