This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

62/100

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Brain scans and imaging

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Alzheimer's disease (AD) is characterized by the brain accumulation of amyloid-β and tau proteins. A growing body of literature suggests that epigenetic dysregulations play a role in the interplay of hallmark proteinopathies with neurodegeneration and cognitive impairment. Here, we aim to characterize an epigenetic dysregulation associated with the brain deposition of amyloid-β and tau proteins. Using positron emission tomography (PET) tracers selective for amyloid-β, tau, and class I histone deacetylase (HDAC I isoforms 1-3), we find that HDAC I levels are reduced in patients with AD. HDAC I PET reduction is associated with elevated amyloid-β PET and tau PET concentrations. Notably, HDAC I reduction mediates the deleterious effects of amyloid-β and tau on brain atrophy and cognitive impairment. HDAC I PET reduction is associated with 2-year longitudinal neurodegeneration and cognitive decline. We also find HDAC I reduction in the postmortem brain tissue of patients with AD and in a transgenic rat model expressing human amyloid-β plus tau pathology in the same brain regions identified in vivo using PET. These observations highlight HDAC I reduction as an element associated with AD pathophysiology.

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

APA 7th

Pascoal, T. A., Chamoun, M., Lax, E., Wey, H. Y., Shin, M., Ng, K. P., et al. (2022). [11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer's disease. Nature communications. https://doi.org/10.1038/s41467-022-30653-5

Vancouver

Pascoal TA, Chamoun M, Lax E, Wey HY, Shin M, Ng KP, et al. [11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer's disease. Nature communications. 2022. doi:10.1038/s41467-022-30653-5. PMID: 35853847.

BibTeX

@article{pascoal2022-35853847,
  author  = {Pascoal, T. A. and Chamoun, M. and Lax, E. and Wey, H. Y. and Shin, M. and Ng, K. P. and Kang, M. S. and Mathotaarachchi, S. and others},
  title   = {{[11C]Martinostat PET analysis reveals reduced HDAC I availability in Alzheimer's disease}},
  journal = {Nature communications},
  year    = {2022},
  doi     = {10.1038/s41467-022-30653-5},
  pmid    = {35853847},
  url     = {https://doi.org/10.1038/s41467-022-30653-5}
}

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's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

How to read this study

Design: this is a follow-up (cohort) study. People are observed over time and not assigned to anything, so an association can reflect other differences between groups. Look at how long follow-up lasted, how many dropped out, and whether the authors adjusted for age, education and other health conditions.
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 moderate. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Moderate means the abstract mentions a cohort, case-control or longitudinal design. 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.

New to reading papers? Six questions to ask of any Alzheimer’s study · how we score.

Key findings

A growing body of literature suggests that epigenetic dysregulations play a role in the interplay of hallmark proteinopathies with neurodegeneration and cognitive impairment.
Here, we aim to characterize an epigenetic dysregulation associated with the brain deposition of amyloid-β and tau proteins.
HDAC I PET reduction is associated with elevated amyloid-β PET and tau PET concentrations.
HDAC I PET reduction is associated with 2-year longitudinal neurodegeneration and cognitive decline.
These observations highlight HDAC I reduction as an element associated with AD pathophysiology.

New to this subject? Start with our plain-English guide: Brain scans & tests →

Study details

Study designlongitudinal study
Evidence strengthModerate

How this study scored 62/100

Published in a leading specialty journal, and it is a longitudinal study following the same people over time. Scored zero for 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 and multicenter collaboration, so those were left out: it earned 36 of the 58 points we could judge it on, which is 62 out of 100.

Component	Points	Why
Journal tier	9 / 10	Tier 2 — leading specialty journal (Nature communications)
Journal's citation record	— / 4	No journal record from OpenAlex — left out of this score
Study design	7 / 12	A longitudinal study following the same people over time
Strength of evidence	3 / 5	Rated “moderate” 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 35853847)
Free to read	2 / 2	Free to read
Points	36 / 58	Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 36 of the 58 points we could judge it on is 62 out of 100.
Total	62 / 100	—

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

Read the original

Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.

Studies in the library that share something with this one. The line above each title says what.

Related studies in Brain scans and imaging from nearby years

Also tagged “reduced”

4 studies in the library carry the topic tag “reduced”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 4 tagged studies.

Studies sharing this one's topic tags

Similar studies

More on Brain scans and imaging

See all studies in Brain scans and imaging →