Evidence map›Paper›PMID 30630081›Full record

ArticleNeuroImage2019

Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model.

Christopher Nishioka, Hsiao-Fang Liang, Barsam Barsamian, Shu-Wei Sun

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in NeuroImage, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Alzheimer's disease: an axonal injury disease?Frontiers in aging neuroscience · 2023
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Magnetic Resonance Imaging in Tauopathy Animal Models.Frontiers in aging neuroscience · 2021
    Review
  17. Retinal Degeneration and Alzheimer's Disease: An Evolving Link.International journal of molecular sciences · 2020
    Review
  18. Review
  19. 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

4 authors at 2 institutions in 1 country.

Christopher NishiokaBasic Sciences, School of Medicine, Loma Linda University, CA, USA; Neuroscience Graduate Program, University of California, Riverside, USA.
Hsiao-Fang LiangBasic Sciences, School of Medicine, Loma Linda University, CA, USA.
Barsam BarsamianBasic Sciences, School of Medicine, Loma Linda University, CA, USA; Neuroscience Graduate Program, University of California, Riverside, USA.
Shu-Wei SunBasic Sciences, School of Medicine, Loma Linda University, CA, USA; Neuroscience Graduate Program, University of California, Riverside, USA; Pharmaceutical Science, School of Pharmacy, Loma Linda University, CA, USA. Electronic address: rsun@llu.edu.
University of California, Riverside · USLoma Linda University · US

Funding

Understanding neuronal and axonal degeneration in a murine model of human MSR01NS062830 · NINDS · LOMA LINDA UNIVERSITY · PI SUN, SHU-WEI · 2011 to 2014
$1.3M
NINDS NIH HHS R01 NS062830
6 · The paper itself

Abstract

White matter abnormalities, revealed by Diffusion Tensor Imaging (DTI), are observed in patients with Alzheimer's Disease (AD), representing neural network deficits that underlie gradual cognitive decline in patients. However, how DTI changes related to the development of Amyloid beta (Aβ) and tau pathology, two key hallmarks of AD, remain elusive. We hypothesized that tauopathy induced by Aβ could initiate an axonal degeneration, leading to DTI-detectable white matter abnormalities. We utilized the visual system of the transgenic p301L tau mice as a model system. Aβ was injected in Lateral Geniculate Nucleus (LGN), where the Retinal Ganglion Cell (RGC) axons terminate. Longitudinal DTI was conducted to detect changes in the optic tract (OT) and optic nerve (ON), containing the distal and proximal segments of RGC axons, respectively. Our results showed DTI changes in OT (significant 13.2% reduction in axial diffusion, AxD vs. vehicle controls) followed by significant alterations in ON AxD and fractional anisotropy, FA. Histology data revealed loss of synapses, RGC axons and cell bodies resulting from the Aβ injection. We further tested whether microtubule-stabilizing compound Epothilone D (EpoD) could ameliorate the damage. EpoD co-treatment with Aβ was sufficient to prevent Aβ-induced axon and cell loss. Using an acute injection paradigm, our data suggest that EpoD may mediate its protective effect by blocking localized, acute Aβ-induced tau phosphorylation. This study demonstrates white matter disruption resulting from localized Aβ, the importance of tau pathology induction to changes in white matter connectivity, and the use of EpoD as a potential therapeutic avenue to prevent the axon loss in AD.

Indexed as

Nerve DegenerationTauopathiesWhite MatterAmyloid beta-PeptidesAnimalsDiffusion Tensor ImagingDisease Models, AnimalEpothilonesGeniculate BodiesMicePeptide FragmentsRetinal Ganglion CellsTubulin ModulatorsAmyloid beta-Peptidesamyloid beta-protein (1-42)desoxyepothilone BEpothilonesPeptide FragmentsTubulin ModulatorsAmyloid betaDiffusion tensor imagingEpoDp301L tauRetinal ganglion cellRetrograde degeneration

Identifiers

PMID30630081
PMCPMC6422724
OpenAlexW2908873665

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.