Air pollution, glymphatic impairment, and Alzheimer's disease

Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt

Epidemiological evidence demonstrates a link between air pollution exposure and the onset and progression of cognitive impairment and Alzheimer's disease (AD). However, current understanding of the underlying pathophysiological mechanisms is limited. This opinion article examines the hypothesis that air pollution-induced impairment of glymphatic clearance represents a crucial etiological event in the development of AD. Exposure to airborne particulate matter (PM) leads to systemic inflammation and neuroinflammation, increased metal load, respiratory and cardiovascular dysfunction, and sleep abnormalities. All these factors are known to reduce the efficiency of glymphatic clearance. Rescuing glymphatic function by restricting the impact of causative agents, and improving sleep and cardiovascular system health, may increase the efficiency of waste metabolite clearance and subsequently slow the progression of AD. In sum, we introduce air pollution-mediated glymphatic impairment as an important mechanistic factor to be considered when interpreting the etiology and progression of AD as well as its responsiveness to therapeutic interventions.
OriginalsprogEngelsk
TidsskriftTrends in Neurosciences
Vol/bind46
Udgave nummer11
Sider (fra-til)901-911
Antal sider11
ISSN0166-2236
DOI
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
We thank Dan Xue for her expert graphical assistance. Funding was provided by the EU Horizon 2020 Research and Innovation Program under grant 814978, National Institutes of Health grants R01AT011439, U19NS128613, R01NS100366, R01AG083020, and P30ES001247, Human Frontier Science Program grant RGP0036, the Dr Miriam and Sheldon G. Adelson Medical Research Foundation, Simons Foundation grant 811237, Lundbeck Foundation grant R386-2021-165, Novo Nordisk Foundation grant NNF20OC0066419, US Army Research Office grant MURI W911NF1910280, and Defense for Health Affairs under the Peer-Reviewed Alzheimer's Research Program through awards W81XWH-22-1-0676 and W81XWH-16-1-0555. Opinions, interpretations, conclusions, and recommendations are those of the authors and are not necessarily endorsed by the Department of Defense. M.N. serves on the Advisory Board of Trends in Neurosciences. The authors declare no competing interests in relation to this work.

Funding Information:
We thank Dan Xue for her expert graphical assistance. Funding was provided by the EU Horizon 2020 Research and Innovation Program under grant 814978 , National Institutes of Health grants R01AT011439 , U19NS128613 , R01NS100366 , R01AG083020 , and P30ES001247 , Human Frontier Science Program grant RGP0036 , the Dr Miriam and Sheldon G. Adelson Medical Research Foundation, Simons Foundation grant 811237 , Lundbeck Foundation grant R386-2021-165 , Novo Nordisk Foundation grant NNF20OC0066419 , US Army Research Office grant MURI W911NF1910280 , and Defense for Health Affairs under the Peer-Reviewed Alzheimer's Research Program through awards W81XWH-22-1-0676 and W81XWH-16-1-0555 . Opinions, interpretations, conclusions, and recommendations are those of the authors and are not necessarily endorsed by the Department of Defense.

Publisher Copyright:
© 2023

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