Evidence map›Paper›PMID 27109181›Full record

ArticleExperimental neurology2016

Amyloid-β plaques disrupt axon initial segments.

Miguel A Marin, Jokubus Ziburkus, Joanna Jankowsky, Matthew N Rasband

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.9field-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

44 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. The Primary Cilia are Associated with the Axon Initial Segment in Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Cellular and pathological functions of tau.Nature reviews. Molecular cell biology · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Node of Ranvier as an Interface for Axo-Glial Interactions: Perturbation of Axo-Glial Interactions in Various Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Review
  15. Article
  16. Review
  17. Review
  18. The Amyloid Precursor Protein Modulates the Position and Length of the Axon Initial Segment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Miguel A MarinDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Jokubus ZiburkusDepartment of Biology and Biochemistry, University of Houston, Houston, TX 77204, USA.
Joanna JankowskyDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Matthew N RasbandDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. Electronic address: rasband@bcm.edu.
Baylor College of Medicine · USUniversity of Houston · US

Funding

Neuroglial Interactions at the Node of RanvierR01NS044916 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI RASBAND, MATTHEW N · 2002 to 2020
$4.2M
Mechanisms of CNS node of Ranvier formation.R01NS069688 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI RASBAND, MATTHEW N · 2010 to 2019
$3.4M
Neuroglial interactions at the node of RanvierR37NS044916 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI RASBAND, MATTHEW N · 2012 to 2018
$2.9M
Selective neuronal silencing to study cognitive decline in Alzheimer's diseaseDP2OD001734 · OD · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI JANKOWSKY, JOANNA L · 2007 to 2010
$2.4M
NIH HHS DP2 OD001734NINDS NIH HHS R01 NS044916NINDS NIH HHS R01 NS069688NINDS NIH HHS R37 NS044916
6 · The paper itself

Abstract

unlabelledAmyloid-β (Aβ) plaques are one of the central pathologies of Alzheimer's disease (AD). Plaque formation in animal models of AD coincides with the appearance of synaptic abnormalities, aberrant neuronal excitability, and cognitive decline. Aβ plaques may disrupt neuronal excitability since they have been proposed to be synaptotoxic, to induce axonal varicosities and neurite breakage, and to significantly decrease spine density. Axon initial segments (AIS) also regulate neuronal excitability and help maintain neuronal polarity. Despite these essential functions, the effects of plaques on AIS structure have not been fully determined. Using a mouse AD model, we measured a significant decrease in the density of AIS up to 75μm away from the center of fibrillar, thioflavin-labeled plaques. The reduction was observed in animals with both moderate and severe plaque loads, and was associated with increased densities of microglia near the plaques. Furthermore, animals with severe plaque loads had significantly reduced AIS lengths adjacent to Aβ plaques. These results suggest the local environment surrounding Aβ plaques may be harmful to the AIS. We propose that AIS loss is a previously unappreciated consequence of AD that could significantly impact brain function. SIGNIFICANCE STATEMENT: This paper demonstrates that neurons near Aβ plaques have disrupted axon initial segments. Loss or disruption of AIS is predicted to have detrimental consequences for brain function.

Indexed as

Age FactorsAlzheimer DiseaseAmyloid beta-Protein PrecursorAnalysis of VarianceAnimalsAxon Initial SegmentBrainCalcium-Calmodulin-Dependent Protein Kinase Type 1Cell Adhesion MoleculesDisease Models, AnimalFemaleHumansIon ChannelsMaleMiceMice, TransgenicAmyloid beta-Protein PrecursorCalcium-Calmodulin-Dependent Protein Kinase Type 1Cell Adhesion MoleculesIon ChannelsNerve Tissue ProteinsAlzheimer'sAxonDegenerationIon channel

Identifiers

PMID27109181
PMCPMC4877279
OpenAlexW2344242115

What OpenQuestion holds

Textmetadata
LicenceTDM
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.