Evidence map›Paper›PMID 23089603›Full record

ReviewReviews in the neurosciences2012

Neurologic and motor dysfunctions in APP transgenic mice.

Robert Lalonde, Ken-Ichiro Fukuchi, Catherine Strazielle

Open access · greenAbstract readReview
In one paragraph

Review in Reviews in the neurosciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 59 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Robert LalondeDepartement de Psychologie, Universite de Rouen, Mont-Saint-Aignan, France. robert.lalonde@univ-rouen.fr
Ken-Ichiro Fukuchi
Catherine Strazielle
Université de Lorraine · FRUniversité de Rouen Normandie · FR

Funding

Innate immunity in Alzheimer's disease: Role of toll-like receptor signalingR01AG030399 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FUKUCHI, KEN-ICHIRO · 2009 to 2013
$1.5M
NIA NIH HHS AG030399NIA NIH HHS R01 AG030399
6 · The paper itself

Abstract

The discovery of gene mutations underlying autosomal dominant Alzheimer's disease has enabled researchers to reproduce several hallmarks of this disorder in transgenic mice, notably the formation of Aβ plaques in brain and cognitive deficits. APP transgenic mutants have also been investigated with respect to survival rates, neurologic functions, and motor coordination, which are all susceptible to alteration in Alzheimer dementia. Several transgenic lines expressing human mutated or wild-type APP had higher mortality rates than non-transgenic controls with or without the presence of Aβ plaques. Mortality rates were also elevated in APP transgenic mice with vascular amyloid accumulation, thereby implicating cerebrovascular factors in the precocious death observed in all APP transgenic models. In addition, myoclonic jumping has been described in APP mutants, together with seizure activity, abnormal limb-flexion and paw-clasping reflexes, and motor coordination deficits. The neurologic signs resemble the myoclonic movements, epileptic seizures, pathological reflexes, and gait problems observed in late-stage Alzheimer's disease.

Indexed as

Amyloid beta-Protein PrecursorAnimalsBrainDisease Models, AnimalGenetic Predisposition to DiseaseHumansMiceMice, TransgenicMovement DisordersMutationNervous System DiseasesAmyloid beta-Protein Precursor

Identifiers

PMID23089603
PMCPMC3481185
OpenAlexW2053487887

What OpenQuestion holds

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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.