Evidence map›Paper›PMID 25241929›Full record

ArticleNature communications2014

PICALM modulates autophagy activity and tau accumulation.

Kevin Moreau, Angeleen Fleming, Sara Imarisio, Ana Lopez Ramirez, Jacob L Mercer, Maria Jimenez-Sanchez, Carla F Bento, Claudia Puri, Eszter Zavodszky, Farah Siddiqi and 5 more

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

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 3 pooled it
12.2field-weighted citation impact, top 1% 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

153 citing papers in PubMed, 3 syntheses or guidelines pooled it, 274 citations in OpenAlex.

  1. Guideline
  2. Pooled it
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  4. Review
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  6. Article
  7. Article
  8. Article
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  11. Regulation of autophagy-mediated pathways by diet, physical activity, and sleep in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  12. Review
  13. Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
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93 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

Kevin MoreauDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Angeleen Fleming1] Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK [2] Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK.
Sara ImarisioDepartment of Genetics, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK.
Ana Lopez Ramirez1] Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK [2] Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK.
Jacob L Mercer1] Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Maria Jimenez-SanchezDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Carla F BentoDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Claudia PuriDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Eszter ZavodszkyDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Farah SiddiqiDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Catherine P LavauDepartment of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710, USA.
Maureen Betton1] Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK [2] Department of Genetics, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK.
Cahir J O'KaneDepartment of Genetics, University of Cambridge, Downing Street, Cambridge CB2 3EG, UK.
Daniel S Wechsler1] Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
David C RubinszteinDepartment of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
University of Cambridge · GBAddenbrooke's Hospital · GBDuke University Hospital · USDuke Medical Center · US

Funding

Mechanisms of Leukemogenic Transformation by MLL-CALMR01CA109281 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WECHSLER, DANIEL STEVEN · 2005 to 2009
$1.3M
Medical Research Council MC_G1000734NCI NIH HHS R01 CA 109281NCI NIH HHS R01 CA109281Wellcome Trust 089703Wellcome Trust 095317Wellcome Trust 100140
6 · The paper itself

Abstract

Genome-wide association studies have identified several loci associated with Alzheimer's disease (AD), including proteins involved in endocytic trafficking such as PICALM/CALM (phosphatidylinositol binding clathrin assembly protein). It is unclear how these loci may contribute to AD pathology. Here we show that CALM modulates autophagy and alters clearance of tau, a protein which is a known autophagy substrate and which is causatively linked to AD, both in vitro and in vivo. Furthermore, altered CALM expression exacerbates tau-mediated toxicity in zebrafish transgenic models. CALM influences autophagy by regulating the endocytosis of SNAREs, such as VAMP2, VAMP3 and VAMP8, which have diverse effects on different stages of the autophagy pathway, from autophagosome formation to autophagosome degradation. This study suggests that the AD genetic risk factor CALM modulates autophagy, and this may affect disease in a number of ways including modulation of tau turnover.

Indexed as

AutophagyAnimalsAutophagy-Related Protein 12Cell LineDrosophilaEndocytosisFemaleFibroblastsGenome-Wide Association StudyHEK293 CellsHeLa CellsHumansMaleMiceMonomeric Clathrin Assembly ProteinsPhagosomesATG12 protein, humanAutophagy-Related Protein 12Monomeric Clathrin Assembly ProteinsPICALM protein, humanRNA, Small InterferingSmall Ubiquitin-Related Modifier Proteinstau ProteinsVAMP2 protein, humanVesicle-Associated Membrane Protein 2

Identifiers

PMID25241929
PMCPMC4199285
OpenAlexW2142222850

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.