Evidence map›Paper›PMID 35146484›Full record

ArticleIBRO neuroscience reports2022

Lysosomal gene

Lauren S Whyte, Célia Fourrier, Sofia Hassiotis, Adeline A Lau, Paul J Trim, Leanne K Hein, Kathryn J Hattersley, Julien Bensalem, John J Hopwood, Kim M Hemsley and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in IBRO neuroscience reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Article
  5. Article
  6. Observational
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  8. Article
  9. The dense-core plaques of Alzheimer's disease are granulomas.The Journal of experimental medicine · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Lauren S WhyteThe University of Adelaide, School of Medicine, North Terrace, Adelaide, SA, Australia.
Célia FourrierLysosomal Health in Ageing, Hopwood Centre for Neurobiology, Lifelong Health Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide, SA, Australia.
Sofia HassiotisLysosomal Health in Ageing, Hopwood Centre for Neurobiology, Lifelong Health Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide, SA, Australia.
Adeline A LauThe University of Adelaide, School of Medicine, North Terrace, Adelaide, SA, Australia.
Paul J TrimProteomics, Metabolomics and MS-Imaging Core Facility, South Australian Health and Medical Research Institute, North Terrace, Adelaide, SA, Australia.
Leanne K HeinLysosomal Health in Ageing, Hopwood Centre for Neurobiology, Lifelong Health Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide, SA, Australia.
Kathryn J HattersleyLysosomal Health in Ageing, Hopwood Centre for Neurobiology, Lifelong Health Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide, SA, Australia.
Julien BensalemLysosomal Health in Ageing, Hopwood Centre for Neurobiology, Lifelong Health Theme, South Australian Health and Medical Research Institute, North Terrace, Adelaide, SA, Australia.
John J HopwoodThe University of Adelaide, School of Medicine, North Terrace, Adelaide, SA, Australia.
Kim M HemsleyThe University of Adelaide, School of Medicine, North Terrace, Adelaide, SA, Australia.
Timothy J SargeantThe University of Adelaide, School of Medicine, North Terrace, Adelaide, SA, Australia.
South Australian Health and Medical Research Institute · AUUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysosomal network abnormalities are an increasingly recognised feature of Alzheimer's disease (AD), which appear early and are progressive in nature. Sandhoff disease and Tay-Sachs disease (neurological lysosomal storage diseases caused by mutations in genes that code for critical subunits of β-hexosaminidase) result in accumulation of amyloid-β (Aβ) and related proteolytic fragments in the brain. However, experiments that determine whether mutations in genes that code for β-hexosaminidase are risk factors for AD are currently lacking. To determine the relationship between β-hexosaminidase and AD, we investigated whether a heterozygous deletion of

Indexed as

AD, Alzheimer’s diseaseAlzheimer’s diseaseAPP, amyloid precursor proteinAppNL-G-F/NL-G-FAβ, amyloid betaCD68, cluster of differentiation 68DementiaELISA, enzyme-linked immunosorbent assayGFAP, glial fibrillary acidic proteinHexbHEXB, β-hexosaminidase β subunitIBA1, ionised calcium binding adaptor molecule 1IL, interleukinKnock-inLAMP1, lysosome associated membrane protein 1LSDs, lysosomal storage disordersLysosomePBS, phosphate buffered salineTREM2, triggering receptor expressed on myeloid cells 2β-hexosaminidase

Identifiers

PMID35146484
PMCPMC8819126
OpenAlexW4206220281

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.