Evidence map›Paper›PMID 10934251›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

Neuropathology in mice expressing human alpha-synuclein.

H van der Putten, K H Wiederhold, A Probst, S Barbieri, C Mistl, S Danner, S Kauffmann, K Hofele, W P Spooren, M A Ruegg and 5 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 1 pooled it
31.2field-weighted citation impact, top 1% 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

179 citing papers in PubMed, 1 synthesis or guideline pooled it, 506 citations in OpenAlex.

  1. Pooled it
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  15. α-Synuclein Pathology and Reduced Neurogenesis in the Olfactory System Affect Olfaction in a Mouse Model of Parkinson's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  16. Article
  17. Review
  18. NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023
    Review
  19. Review
  20. Article

119 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

15 authors at 1 institution in 1 country.

H van der PuttenNervous System Research, Novartis Pharma Inc., CH 4002 Basel, Switzerland. p_herman.van_der_putten@pharma.novartis.com
K H Wiederhold
A Probst
S Barbieri
C Mistl
S Danner
S Kauffmann
K Hofele
W P Spooren
M A Ruegg
S Lin
P Caroni
B Sommer
M Tolnay
G Bilbe
Novartis (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The presynaptic protein alpha-synuclein is a prime suspect for contributing to Lewy pathology and clinical aspects of diseases, including Parkinson's disease, dementia with Lewy bodies, and a Lewy body variant of Alzheimer's disease. alpha-Synuclein accumulates in Lewy bodies and Lewy neurites, and two missense mutations (A53T and A30P) in the alpha-synuclein gene are genetically linked to rare familial forms of Parkinson's disease. Under control of mouse Thy1 regulatory sequences, expression of A53T mutant human alpha-synuclein in the nervous system of transgenic mice generated animals with neuronal alpha-synucleinopathy, features strikingly similar to those observed in human brains with Lewy pathology, neuronal degeneration, and motor defects, despite a lack of transgene expression in dopaminergic neurons of the substantia nigra pars compacta. Neurons in brainstem and motor neurons appeared particularly vulnerable. Motor neuron pathology included axonal damage and denervation of neuromuscular junctions in several muscles examined, suggesting that alpha-synuclein interfered with a universal mechanism of synapse maintenance. Thy1 transgene expression of wild-type human alpha-synuclein resulted in similar pathological changes, thus supporting a central role for mutant and wild-type alpha-synuclein in familial and idiotypic forms of diseases with neuronal alpha-synucleinopathy and Lewy pathology. These mouse models provide a means to address fundamental aspects of alpha-synucleinopathy and test therapeutic strategies.

Indexed as

alpha-SynucleinAnimalsCentral Nervous SystemGene Expression RegulationHumansLewy BodiesMiceMice, TransgenicMotor ActivityMotor NeuronsMovement DisordersMutationNerve DegenerationNerve Tissue ProteinsNeurodegenerative DiseasesPsychomotor Performancealpha-SynucleinNerve Tissue ProteinsSNCA protein, humanSnca protein, mouseSynucleins

Identifiers

PMID10934251
PMCPMC6772584
OpenAlexW2056823686

What OpenQuestion holds

Textmetadata
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.