Evidence map›Paper›PMID 19111542›Full record

ArticleExperimental neurology2009

Neuritic dystrophy and neuronopathy in Akita (Ins2(Akita)) diabetic mouse sympathetic ganglia.

Robert E Schmidt, Karen G Green, Lisa L Snipes, Dongyan Feng

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Neurobiological Opportunities in Diabetic Polyneuropathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Synapses on sympathetic neurons and parasympathetic neurons differ in their vulnerability to diabetes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  17. Article
  18. Article
  19. Retinal angiogenesis in the Ins2(Akita) mouse model of diabetic retinopathy.Investigative ophthalmology & visual science · 2013
    Article
  20. 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 1 institution in 1 country.

Robert E SchmidtDivision of Neuropathology, Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO 63110, USA. reschmidt@wustl.edu
Karen G Green
Lisa L Snipes
Dongyan Feng
Washington University in St. Louis · US

Funding

NEUROPATHOLOGY OF THE AGING SYMPATHETIC NERVOUS SYSTEMR01AG010299 · NIA · WASHINGTON UNIVERSITY · PI SCHMIDT, ROBERT EDWARD · 1992 to 2006
$1.7M
EXPERIMENTAL DIABETIC AUTONOMIC NEUROPATHYR37DK019645 · NIDDK · WASHINGTON UNIVERSITY · PI SCHMIDT, ROBERT EDWARD · 1999 to 2004
$1.6M
EXPERIMENTAL DIABETIC AUTONOMIC NEUROPATHYR01DK019645 · NIDDK · WASHINGTON UNIVERSITY · PI SCHMIDT, ROBERT EDWARD · 1986 to 2010
$1.3M
NIA NIH HHS AG10299NIA NIH HHS R01 AG010299NIDDK NIH HHS R01 DK019645NIDDK NIH HHS R37 DK019645NIDDK NIH HHS R37 DK19645
6 · The paper itself

Abstract

Diabetic autonomic neuropathy is a debilitating, poorly studied complication of diabetes. Our previous studies of non-obese diabetic (NOD) and related mouse models identified rapidly developing, dramatic pathology in prevertebral sympathetic ganglia; however, once diabetic, the mice did not survive for extended periods needed to examine the ability of therapeutic agents to correct established neuropathy. In the current manuscript we show that the Akita (Ins2(Akita)) mouse is a robust model of diabetic sympathetic autonomic neuropathy with unambiguous, spontaneous, rapidly-developing neuropathology which corresponds closely to the characteristic pathology of other rodent models and man. Akita mice diabetic for 2, 4 or 8 months of diabetes progressively developed markedly swollen axons and dendrites ("neuritic dystrophy") in the prevertebral superior mesenteric (SMG) and celiac ganglia (CG). Comparable changes failed to develop in the superior cervical ganglia (SCG) of the Akita mouse or in any ganglia of non-diabetic mice. Morphometric studies demonstrate an overall increase in presynaptic axon terminal cross sectional area, including those without any ultrastructural features of dystrophy. Neurons in Akita mouse prevertebral sympathetic ganglia show an unusual perikaryal alteration characterized by the accumulation of membranous aggregates and minute mitochondria and loss of rough endoplasmic reticulum. These changes result in the loss of a third of neurons in the CG over the course of 8 months of diabetes. The extended survival of diabetic mice and robust pathologic findings provide a clinically relevant paradigm that will facilitate the analysis of novel therapeutic agents on the reversal of autonomic neuropathy.

Indexed as

AnimalsAxonsDendritesDiabetic NeuropathiesDisease Models, AnimalDisease ProgressionEndoplasmic Reticulum, RoughGanglia, SympatheticMiceMice, Inbred C57BLMice, Mutant StrainsMice, TransgenicMicroscopy, Electron, TransmissionMitochondriaNerve DegenerationNeurons

Identifiers

PMID19111542
PMCPMC2672346
OpenAlexW2026758511

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.