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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.

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Genetics

Topic: Brain proteins, microglia and lab models

Neurodegenerative pathologies associated with aging exhibit clinical and morphological features that are relatively specific to humans. To gain insights into the evolution of the regulatory mechanisms of the aged brain, we compared age-related differences in microRNA (miRNA) expression levels in the cortex and cerebellum of humans, chimpanzees and rhesus macaques on a genome-wide scale. In contrast to global miRNA downregulation, a small subset of miRNAs was found to be selectively upregulated in the aging brain of all 3 species. Notably, miR-144 that is highly conserved appeared to be associated with the aging progression. Moreover, miR-144 plays a central role in regulating the expression of ataxin 1 (ATXN1), the disease-causing gene for the development spinocerebellar ataxia type 1 (SCA1). miRNA activity, including miR-144, -101 and -130 processing, was increased in the cerebellum and cortex of SCA1 and Alzheimer patients relative to healthy aged brains. Importantly, miR-144 and -101 inhibition increased ATXN1 levels in human cells. Thus, the activation of miRNA expression in the aging brain may serve to reduce the cytotoxic effect of polyglutamine expanded ATXN1 and the deregulation of miRNA expression may be a risk factor for disease development.

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

APA 7th

Persengiev, S., Kondova, I., Otting, N., Koeppen, A. H., & Bontrop, R. E. (2011). Genome-wide analysis of miRNA expression reveals a potential role for miR-144 in brain aging and spinocerebellar ataxia pathogenesis. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2010.03.014

Vancouver

Persengiev S, Kondova I, Otting N, Koeppen AH, Bontrop RE. Genome-wide analysis of miRNA expression reveals a potential role for miR-144 in brain aging and spinocerebellar ataxia pathogenesis. Neurobiology of aging. 2011. doi:10.1016/j.neurobiolaging.2010.03.014. PMID: 20451302.

BibTeX

@article{persengiev2011-20451302,
  author  = {Persengiev, S. and Kondova, I. and Otting, N. and Koeppen, A. H. and Bontrop, R. E.},
  title   = {{Genome-wide analysis of miRNA expression reveals a potential role for miR-144 in brain aging and spinocerebellar ataxia pathogenesis}},
  journal = {Neurobiology of aging},
  year    = {2011},
  doi     = {10.1016/j.neurobiolaging.2010.03.014},
  pmid    = {20451302},
  url     = {https://doi.org/10.1016/j.neurobiolaging.2010.03.014}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

Key findings

Why it matters

This study compared microRNA expression in the aging brains of humans, chimpanzees and macaques, and found that miR-144 is linked to aging and regulates the gene that causes spinocerebellar ataxia type 1. In cells, blocking miR-144 and miR-101 raised ATXN1 levels, suggesting that miRNA activity in the aging brain may help reduce the toxic effects of this protein, though this is early laboratory work.

Study details

How this study scored 40/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 3 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 5 of 7; Citations per year 3 of 5; Impact for its field and year 2 of 6; Cited by studies here 1 of 6; Still being cited 1 of 4; Senior author's track record 3 of 4; Institution's track record 0 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 40 of 100.40 of 100 points earned60 not earned

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Neurobiology of aging)
Journal's citation record 3 / 4 Neurobiology of Aging: journal h-index 263 (OpenAlex, 2026-10-29)
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 1 / 5 2011 — within 20 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)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 5 / 7 Cited 143 times (OpenAlex, 2026-10-10)
Citations per year 3 / 5 8.4 citations a year over 17 year(s) since 2011
Impact for its field and year 2 / 6 Cited 2.6× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 1 / 6 Cited by 1 other studies in this library
Still being cited 1 / 4 Cited 14 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 3 / 4 Last-listed author Ronald E. Bontrop: h-index 70 (OpenAlex, whole career)
Institution's track record 0 / 3 Biomedical Primate Research Centre: institution h-index 179 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 2 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 20451302)
Free to read 0 / 2 Behind a paywall — scores zero
Total 40 / 100 —

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

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