Evidence map›Paper›PMID 24412275›Full record

ReviewBiochemical pharmacology2014

Is synaptic loss a unique hallmark of Alzheimer's disease?

Stephen W Scheff, Janna H Neltner, Peter T Nelson

Abstract readReview
In one paragraph

Review in Biochemical pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

81 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Celebrating 40 years of the University of Kentucky Alzheimer's Disease Research Center.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. 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
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Alzheimer's disease: an axonal injury disease?Frontiers in aging neuroscience · 2023
    Review
  19. Article
  20. Article

21 more citing papers are in PubMed but not listed here.

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

3 authors.

Stephen W ScheffDepartment of Anatomy and Neurobiology, University of Kentucky Medical Center, University of Kentucky, Lexington, KY 40536, United States; Sanders-Brown Center on Aging and Alzheimer's Disease Center, University of Kentucky Medical Center, University of Kentucky, Lexington, KY 40536, United States. Electronic address: sscheff@email.uky.edu.
Janna H NeltnerDepartment of Pathology and Division of Neuropathology, University of Kentucky Medical Center, University of Kentucky, Lexington, KY 40536, United States.
Peter T NelsonSanders-Brown Center on Aging and Alzheimer's Disease Center, University of Kentucky Medical Center, University of Kentucky, Lexington, KY 40536, United States; Department of Pathology and Division of Neuropathology, University of Kentucky Medical Center, University of Kentucky, Lexington, KY 40536, United States. Electronic address: pnels2@email.uky.edu.

Funding

University of Kentucky Alzheimer's Disease Core Center - Biomarker CoreP30AG028383 · NIA · UNIVERSITY OF KENTUCKY · PI GOLD, BRIAN TIMOTHY, VAN ELDIK, LINDA J · 2006 to 2020
$23.3M
CELLULAR CHANGES ALTERING SYNAPTIC CONNECTIVITY IN PRECLINICAL ADR01AG042475 · NIA · UNIVERSITY OF KENTUCKY · PI NELSON, PETER T. · 2013 to 2017
$1.5M
SYNAPTIC CHANGE IN MILD COGNITIVE IMPAIRMENTR01AG027219 · NIA · UNIVERSITY OF KENTUCKY · PI SCHEFF, STEPHEN W · 2006 to 2010
$1.3M
Alpha-synuclein mRNA is a putative microRNA targetK08NS050110 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI NELSON, PETER T. · 2005 to 2009
$863k
Aperio ScanScope XT Digital Slide Scanner SystemS10RR026489 · NCRR · UNIVERSITY OF KENTUCKY · PI NELSON, PETER T. · 2011 to 2011
$284k
NCRR NIH HHS S10 RR026489NIA NIH HHS 5-P30-AG028383NIA NIH HHS P30 AG028383NIA NIH HHS R01 AG027219NIA NIH HHS R01 AG042475NIA NIH HHS R01AG042475NINDS NIH HHS K08 NS050110
6 · The paper itself

Abstract

Synapses may represent a key nidus for dementia including Alzheimer's disease (AD) pathogenesis. Here we review published studies and present new ideas related to the question of the specificity of synapse loss in AD. Currently, AD is defined by the regional presence of neuritic plaques and neurofibrillary tangles in the brain. The severity of involvement by those pathological hallmarks tends to correlate both with antemortem cognitive status, and also with synapse loss in multiple brain areas. Recent studies from large autopsy series have led to a new standard of excellence with regard to clinical-pathological correlation and to improved comprehension of the numerous brain diseases of the elderly. These studies have provided evidence that it is the rule rather than the exception for brains of aged individuals to demonstrate pathologies (often multiple) other than AD plaques and tangles. For many of these comorbid pathologies, the extent of synapse loss is imperfectly understood but could be substantial. These findings indicate that synapse loss is probably not a hallmark specific to AD but rather a change common to many diseases associated with dementia.

Indexed as

AgingAlzheimer DiseaseAnimalsBrainCognitionDisease Models, AnimalHumansSynapsesCerebrovascularHippocampal sclerosisHS-AgingNeuropathologyTDP-43

Identifiers

PMID24412275
PMCPMC4230706

What OpenQuestion holds

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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.