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41/100

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Risk factors

Topic: Air pollution and environmental exposures

Plain-language summary

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.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Hussain, R., Graham, U., Elder, A., & Nedergaard, M. (2023). Air pollution, glymphatic impairment, and Alzheimer's disease. Trends in neurosciences. https://doi.org/10.1016/j.tins.2023.08.010

Vancouver

Hussain R, Graham U, Elder A, Nedergaard M. Air pollution, glymphatic impairment, and Alzheimer's disease. Trends in neurosciences. 2023. doi:10.1016/j.tins.2023.08.010. PMID: 37777345.

BibTeX

@article{hussain2023-37777345,
  author  = {Hussain, Rashad and Graham, Uschi and Elder, Alison and Nedergaard, Maiken},
  title   = {{Air pollution, glymphatic impairment, and Alzheimer's disease}},
  journal = {Trends in neurosciences},
  year    = {2023},
  doi     = {10.1016/j.tins.2023.08.010},
  pmid    = {37777345},
  url     = {https://doi.org/10.1016/j.tins.2023.08.010}
}

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What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

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.

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Study details

Evidence strengthLow

How this study scored 41/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multicenter collaboration and free to read, so those were left out: it earned 23 of the 56 points we could judge it on, which is 41 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Trends in neurosciences)
Journal's citation record	— / 4	No journal record from OpenAlex — left out of this score
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	3 / 5	2023 — within 6 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	— / 7	No citation count (not found in OpenAlex) — left out of this score
Citations per year	— / 5	No citation count or no year — left out of this score
Impact for its field and year	— / 6	No field-weighted citation impact (OpenAlex has none yet) — left out of this score
Cited by studies here	— / 6	Not yet checked against this library's citation graph — left out of this score
Still being cited	— / 4	No yearly citation counts — left out of this score
Senior author's track record	— / 4	Senior author's record not available — left out of this score
Institution's track record	— / 3	No institution listed in OpenAlex — left out of this score
Multicenter collaboration	— / 3	Institutions not listed — left out of this score
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 37777345)
Free to read	— / 2	Access not recorded — left out of this score
Points	23 / 56	Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 23 of the 56 points we could judge it on is 41 out of 100.
Total	41 / 100	—

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