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43/100

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Disease mechanisms

Topic: Inflammation, microglia and astrocytes

Plain-language summary

Autophagy plays a pivotal role in the pathogenesis and progression of Alzheimer's disease (AD). Oxidative stress and neuroinflammation involved in autophagy are associated with the cerebral ischemia-induced exacerbation of cognitive deficits in individuals with AD. APP/PS1 mice underwent bilateral common carotid artery clamping for 15 min. The degrees of Aβ deposition, oxidative stress, neuroinflammation, and neuronal and synaptic loss after cerebral ischemia were detected. Autophagy levels were assessed by RT-qPCR, western blotting, immunofluorescence staining, and transmission electron microscopy. DPEs occurring in the hippocampus of APP/PS1 mice after cerebral ischemia were analyzed via label-free proteomics. The present study demonstrated that cerebral ischemia exacerbates learning and memory deficits in APP/PS1 mice. Cerebral ischemia aggravated the cognitive impairment in APP/PS1 mice by worsening neuronal and synaptic loss through damage to intracellular autophagy, increased oxidative stress, and neuroinflammation. Notably, cerebral ischemia interfered with mitochondrial and nuclear transport functions in APP/PS1 transgenic mice, thereby aggravating cognitive deficits. Cellular transport functions may be a target for preventing AD progression. In summary, autophagy is impaired in APP/PS1 mice compared with WT mice, and oxidative stress and neuroinflammation caused by cerebral ischemia exacerbate autophagy-induced damage and are responsible for cognitive decline. Label-free proteomics indicated that cerebral ischemia results in abnormal Abcb8, Sestd1, TPR, and Rab8a protein expression in the hippocampus of APP/PS1 transgenic mice and that an imbalance of mitochondrial transport and nuclear transport functions exacerbates cognitive deficits. Improving autophagy and restoring organelle transport may be targets for the prevention and treatment of dementia.

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

APA 7th

Ning, Z., Zhong, X., Wang, Y., Hu, D., Tang, X., & Deng, M. (2024). Cerebral ischemic injury impairs autophagy and exacerbates cognitive impairment in APP/PS1 mice. International immunopharmacology. https://doi.org/10.1016/j.intimp.2024.113581

Vancouver

Ning Z, Zhong X, Wang Y, Hu D, Tang X, Deng M. Cerebral ischemic injury impairs autophagy and exacerbates cognitive impairment in APP/PS1 mice. International immunopharmacology. 2024. doi:10.1016/j.intimp.2024.113581. PMID: 39522311.

BibTeX

@article{ning2024-39522311,
  author  = {Ning, Zhenqiu and Zhong, Xiaoqin and Wang, Yu and Hu, Dafeng and Tang, Xialin and Deng, Minzhen},
  title   = {{Cerebral ischemic injury impairs autophagy and exacerbates cognitive impairment in APP/PS1 mice}},
  journal = {International immunopharmacology},
  year    = {2024},
  doi     = {10.1016/j.intimp.2024.113581},
  pmid    = {39522311},
  url     = {https://doi.org/10.1016/j.intimp.2024.113581}
}

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How to read this study

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Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

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

Oxidative stress and neuroinflammation involved in autophagy are associated with the cerebral ischemia-induced exacerbation of cognitive deficits in individuals with AD.
The present study demonstrated that cerebral ischemia exacerbates learning and memory deficits in APP/PS1 mice.
In summary, autophagy is impaired in APP/PS1 mice compared with WT mice, and oxidative stress and neuroinflammation caused by cerebral ischemia exacerbate autophagy-induced damage and are responsible for cognitive decline.
Label-free proteomics indicated that cerebral ischemia results in abnormal Abcb8, Sestd1, TPR, and Rab8a protein expression in the hippocampus of APP/PS1 transgenic mice and that an imbalance of mitochondrial transport and nuclear transport functions exacerbates cognitive deficits.

Study details

Evidence strengthLow

How this study scored 43/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported 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 24 of the 56 points we could judge it on, which is 43 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (International immunopharmacology)
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	4 / 5	2024 — within 3 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	Laboratory or animal study (title names “app/ps1”) — scores zero
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 39522311)
Free to read	— / 2	Access not recorded — left out of this score
Points	24 / 56	Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 24 of the 56 points we could judge it on is 43 out of 100.
Total	43 / 100	—

What each of these 20 components measures, and what this score is not →

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