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41/100

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Vascular contributions

Topic: Disease mechanisms in lab and animal studies

Plain-language summary

Cerebral amyloid angiopathy (CAA) is characterized by cerebrovascular amyloid β (Aβ) deposits and causes dementia and cerebral hemorrhage. Although α-enolase (ENO1) was shown to possess multifunctional roles, its exact functions in CAA pathogenesis have not been determined. In this study, we focused on ENO1, a well-known glycolytic enzyme, which was previously identified via a proteomic approach as an upregulated protein in brain samples from patients with Alzheimer's disease (AD). We utilized the thioflavin T fluorescence assay and transmission electron microscopy to monitor the effects of ENO1 on amyloid formation by Aβ peptides. We also cultured murine primary cerebrovascular smooth muscle cells to determine the effects of ENO1 on Aβ cytotoxicity. To investigate the effects of ENO1 in vivo, we infused ENO1 or a vehicle control into the brains of APP23 mice, a transgenic model of AD/CAA, using a continuous infusion system, followed by a cognitive test and pathological and biochemical analyses. We found that novel functions of ENO1 included interacting with Aβ and inhibiting its fibril formation, disrupting Aβ fibrils, and weakening the cytotoxic effects of these fibrils via proteolytic degradation of Aβ peptide. We also demonstrated that infusion of ENO1 into APP23 mouse brains reduced cerebrovascular Aβ deposits and improved cognitive impairment. In addition, we found that enzymatically inactivated ENO1 failed to inhibit Aβ fibril formation and fibril disruption. The proteolytic activity of ENO1 may thus underlie the enzyme's cytoprotective effect and clearance of Aβ from the brain, and ENO1 may be a therapeutic target in CAA.

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

APA 7th

Inoue, Y., Tasaki, M., Masuda, T., Misumi, Y., Nomura, T., Ando, Y., et al. (2022). α-Enolase reduces cerebrovascular Aβ deposits by protecting Aβ amyloid formation. Cellular and molecular life sciences : CMLS. https://doi.org/10.1007/s00018-022-04493-x

Vancouver

Inoue Y, Tasaki M, Masuda T, Misumi Y, Nomura T, Ando Y, et al. α-Enolase reduces cerebrovascular Aβ deposits by protecting Aβ amyloid formation. Cellular and molecular life sciences : CMLS. 2022. doi:10.1007/s00018-022-04493-x. PMID: 35916996.

BibTeX

@article{inoue2022-35916996,
  author  = {Inoue, Yasuteru and Tasaki, Masayoshi and Masuda, Teruaki and Misumi, Yohei and Nomura, Toshiya and Ando, Yukio and Ueda, Mitsuharu},
  title   = {{α-Enolase reduces cerebrovascular Aβ deposits by protecting Aβ amyloid formation}},
  journal = {Cellular and molecular life sciences : CMLS},
  year    = {2022},
  doi     = {10.1007/s00018-022-04493-x},
  pmid    = {35916996},
  url     = {https://doi.org/10.1007/s00018-022-04493-x}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
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

We found that novel functions of ENO1 included interacting with Aβ and inhibiting its fibril formation, disrupting Aβ fibrils, and weakening the cytotoxic effects of these fibrils via proteolytic degradation of Aβ peptide.
We also demonstrated that infusion of ENO1 into APP23 mouse brains reduced cerebrovascular Aβ deposits and improved cognitive impairment.
In addition, we found that enzymatically inactivated ENO1 failed to inhibit Aβ fibril formation and fibril disruption.

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 (Cellular and molecular life sciences : CMLS)
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	2022 — 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 35916996)
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	—

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

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