Evidence map›Paper›PMID 37171832›Full record

Observational studyMovement disorders : official journal of the Movement Disorder Society2023

Longitudinal Synaptic Loss in Primary Tauopathies: An In Vivo [

Negin Holland, P Simon Jones, George Savulich, Michelle Naessens, Maura Malpetti, David J Whiteside, Duncan Street, Peter Swann, Young T Hong, Tim D Fryer and 6 more

Open access · hybridAbstract readObservational Study
In one paragraph

Observational study in Movement disorders : official journal of the Movement Disorder Society, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
4.3field-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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Twenty years of therapeutic development in tauopathy mouse models: a scoping review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Synaptic changes in psychiatric and neurological disorders: state-of-the art of in vivo imaging.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Review
  11. Tracing synaptic loss in Alzheimer's brain with SV2A PET-tracer UCB-J.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  12. Article
  13. Article
  14. SV2A PET imaging in human neurodegenerative diseases.Frontiers in aging neuroscience · 2024
    Review
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

16 authors at 3 institutions in 2 countries.

Negin HollandDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0003-3813-0882
P Simon JonesDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.
George SavulichDepartment of Psychiatry, University of Cambridge, School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, United Kingdom.
Michelle NaessensDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.
Maura MalpettiDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0001-8923-9656
David J WhitesideDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0002-5890-9220
Duncan StreetDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.
Peter SwannCambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom.
Young T HongDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.
Tim D FryerDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.
Timothy RittmanDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0003-1063-6937
Eoin MulroyDepartment of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London, United Kingdom.
Franklin I AigbirhioDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.
Kailash P BhatiaDepartment of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London, United Kingdom.ORCID 0000-0001-8185-286X
John T O'BrienCambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom.
James B RoweDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, United Kingdom.ORCID 0000-0001-7216-8679
University of Cambridge · GBNational Hospital for Neurology and Neurosurgery · GBMRC Cognition and Brain Sciences Unit · GB

Funding

Medical Research Council MC-UU-00030/14Medical Research Council MC_UU_00030/14Medical Research Council MR/T033371/1Wellcome TrustWellcome Trust 220258
6 · The paper itself

Abstract

backgroundSynaptic loss is characteristic of many neurodegenerative diseases; it occurs early and is strongly related to functional deficits.

objectiveIn this longitudinal observational study, we determine the rate at which synaptic density is reduced in the primary tauopathies of progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD), and we test the relationship with disease progression.

methodsOur cross-sectional cohort included 32 participants with probable PSP and 16 with probable CBD (all amyloid-negative corticobasal syndrome), recruited from tertiary care centers in the United Kingdom, and 33 sex- and age-matched healthy control subjects. Synaptic density was estimated by positron emission tomography imaging with the radioligand [

resultsWe found significant annual synaptic loss within the frontal lobe (-3.5%, P = 0.03) and the right caudate (-3.9%, P = 0.046). The degree of longitudinal synaptic loss within the frontal lobe correlated with the rate of change in the PSP Rating Scale (R = 0.47, P = 0.03) and cognition (Addenbrooke's Cognitive Examination-Revised, R = -0.62, P = 0.003).

conclusionsWe provide in vivo evidence for rapid progressive synaptic loss, correlating with clinical progression in primary tauopathies. Synaptic loss may be an important therapeutic target and outcome variable for early-phase clinical trials of disease-modifying treatments. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Indexed as

Movement DisordersSupranuclear Palsy, ProgressiveTauopathiesBrainCross-Sectional StudiesHumansPositron-Emission Tomography[11C]UCB-J PETlongitudinalprimary tauopathies

Identifiers

PMID37171832
PMCPMC10947001
OpenAlexW4376226745

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.