Evidence map›Paper›PMID 37580797›Full record

ArticleActa neuropathologica communications2023

Cathepsin B abundance, activity and microglial localisation in Alzheimer's disease-Down syndrome and early onset Alzheimer's disease; the role of elevated cystatin B.

Yixing Wu, Paige Mumford, Suzanna Noy, Karen Cleverley, Alicja Mrzyglod, Dinghao Luo, Floris van Dalen, Martijn Verdoes, Elizabeth M C Fisher, Frances K Wiseman

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Why in vivo models of disease remain indispensable.Disease models & mechanisms · 2026
    Article
  3. Article
  4. Review
  5. Cathepsins in Neurological Diseases.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

10 authors at 3 institutions in 2 countries.

Yixing WuThe UK Dementia Research Institute, University College London, Queen Square, London, WC1N 3BG, UK.
Paige MumfordThe UK Dementia Research Institute, University College London, Queen Square, London, WC1N 3BG, UK.
Suzanna NoyDepartment of Neuromuscular Diseases, Queen Square Institute of Neurology, University College London, Queen Square, London, WC1N 3BG, UK.
Karen CleverleyDepartment of Neuromuscular Diseases, Queen Square Institute of Neurology, University College London, Queen Square, London, WC1N 3BG, UK.
Alicja MrzyglodThe UK Dementia Research Institute, University College London, Queen Square, London, WC1N 3BG, UK.
Dinghao LuoThe UK Dementia Research Institute, University College London, Queen Square, London, WC1N 3BG, UK.
Floris van DalenDepartment of Medical BioSciences, Radboudumc, Geert Grooteplein Zuid 28, 6525 GA, Nijmegen, The Netherlands.
Martijn VerdoesDepartment of Medical BioSciences, Radboudumc, Geert Grooteplein Zuid 28, 6525 GA, Nijmegen, The Netherlands.
Elizabeth M C FisherDepartment of Neuromuscular Diseases, Queen Square Institute of Neurology, University College London, Queen Square, London, WC1N 3BG, UK.
Frances K WisemanThe UK Dementia Research Institute, University College London, Queen Square, London, WC1N 3BG, UK. f.wiseman@ucl.ac.uk.ORCID http://orcid.org/0000-0001-9323-3548
UK Dementia Research Institute · GBNational Hospital for Neurology and Neurosurgery · GBRadboud University Nijmegen · NL

Funding

Wellcome Trust 098328Wellcome Trust 098330/Z/12/Z
6 · The paper itself

Abstract

Cathepsin B is a cysteine protease that is implicated in multiple aspects of Alzheimer's disease pathogenesis. The endogenous inhibitor of this enzyme, cystatin B (CSTB) is encoded on chromosome 21. Thus, individuals who have Down syndrome, a genetic condition caused by having an additional copy of chromosome 21, have an extra copy of an endogenous inhibitor of the enzyme. Individuals who have Down syndrome are also at significantly increased risk of developing early-onset Alzheimer's disease (EOAD). The impact of the additional copy of CSTB on Alzheimer's disease development in people who have Down syndrome is not well understood. Here we compared the biology of cathepsin B and CSTB in individuals who had Down syndrome and Alzheimer's disease, with disomic individuals who had Alzheimer's disease or were ageing healthily. We find that the activity of cathepsin B enzyme is decreased in the brain of people who had Down syndrome and Alzheimer's disease compared with disomic individuals who had Alzheimer's disease. This change occurs independently of an alteration in the abundance of the mature enzyme or the number of cathepsin B

Indexed as

Alzheimer DiseaseDown SyndromeAnimalsCathepsin BCystatin BHumansMiceMicrogliaCathepsin BCystatin BAlzheimer’s diseaseCathepsin BCystatin BDown syndrome

Identifiers

PMID37580797
PMCPMC10426223
OpenAlexW4385802570

What Socratic 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 Socratic graph.