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Consort 2010 statement: extension to cluster randomised trials

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Campbell, M. K., Piaggio, G., Elbourne, D. R., Altman, D. G., for the CONSORT Group·2012·BMJ

DOI 10.1136/bmj.e5661

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Abstract

Abstract In age-related neurodegenerative disease, like Alzheimer’s and Parkinson’s disease, disease-specific proteins become aggregation-prone and form amyloid-like deposits. Depletion of SERF proteins ameliorates this toxic process in worm- and human cell models for disease. Whether SERF modifies amyloid pathology in mammalian brain, however, has remained unknown. Here, we generated SERF2 brain-specific knockout mice which, unlike full body knockout mice, were viable, and showed no major behavioral and cognitive abnormalities. We combined these knockout mice with the APPPS1 mouse model for human amyloid beta aggregation. Using structure-specific amyloid dyes, previously used to distinguish amyloid polymorphisms in human brain, we show that knockout of SERF2 alters the structure of amyloid fibrils and deposits. Moreover, scanning transmission electron microscopy revealed thicker, shorter and more densely packed amyloid in absence of SERF2. Altogether, our data reveal pleiotropic functions of SERF in development and aging and support a function as a modifier of amyloid aggregation in mammalian brain. Our results indicate that single cellular factors like SERF can determine the structural outcome of amyloid aggregation, offering possibilities for polymorphism-based disease interventions.

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Self-citation

Authors: Campbell, M. K., Piaggio, G., Elbourne, D. R., Altman, D. G., & for the CONSORT Group
Affiliations: University of Aberdeen (GB)
London School of Hygiene & Tropical Medicine (GB)
University of Oxford (GB)
Corresponding author: Campbell, M. K.
ORCID: Campbell, M. K.
Piaggio, G.
Altman, D. G.
Venue: BMJ
Publisher: BMJ
Published: 2012-09-04
Volume: 345
Issue: sep04 1
Pages: e5661-e5661
ISSN: 1756-1833 (ISSN-L)
DOI: 10.1136/bmj.e5661
OpenAlex: W2102330235
Cited by: 3,510
References: 131
Citations by year: 2026: 194 · 2025: 227 · 2024: 211 · 2023: 221 · 2022: 248 · 2021: 264 · 2020: 249 · 2019: 172 · 2018: 197 · 2017: 174 · 2016: 172 · 2015: 201 · 2014: 166 · 2013: 165 · 2012: 109
FWCI: 137.68
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: BMJ (publishedVersion)
PubMed (publishedVersion)
Aberdeen University Research Archive (Aberdeen University) (submittedVersion)
Oxford University Research Archive (ORA) (University of Oxford) (submittedVersion)
Funders: U.S. Department of Health and Human Services
Scottish Government
Cancer Research UK (C5529)
National Institutes of Health
Chief Scientist Office, Scottish Government Health and Social Care Directorate
Medical Research Council (MR/J004871/1)
National Cancer Institute
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Physical Sciences › Mathematics › Statistics and Probability › Statistical Methods in Clinical Trials
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: amyloid fibril formation, amyloid fibril structure, Alzheimer's disease, Parkinson's disease, age-related neurodegenerative diseases, amyloid polymorphism, scanning transmission electron microscopy, genetic modifiers
MeSH terms: Data Interpretation, Statistical, Humans, Random Allocation, Cluster Analysis, Randomized Controlled Trials as Topic, Sample Size

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