Does overexpression of betaAPP in aging muscle have a pathogenic role and a relevance to Alzheimer's disease? Clues from inclusion body myositis, cultured human muscle, and transgenic mice.

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.

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.

Who cites it

9 citing papers in PubMed.

1. Activation of the Unfolded Protein Response in Sporadic Inclusion-Body Myositis but Not in Hereditary GNE Inclusion-Body Myopathy.Journal of neuropathology and experimental neurology · 2015
   Article
2. Amyloid-β protein impairs Ca2+ release and contractility in skeletal muscle.Neurobiology of aging · 2010
   Article
3. How citation distortions create unfounded authority: analysis of a citation network.BMJ (Clinical research ed.) · 2009
   Article
4. Inclusion body myositis: a degenerative muscle disease associated with intra-muscle fiber multi-protein aggregates, proteasome inhibition, endoplasmic reticulum stress and decreased lysosomal degradation.Brain pathology (Zurich, Switzerland) · 2009
   Review
5. Inclusion-body myositis: muscle-fiber molecular pathology and possible pathogenic significance of its similarity to Alzheimer's and Parkinson's disease brains.Acta neuropathologica · 2008
   Review
6. MyoD expression restores defective myogenic differentiation of human mesoangioblasts from inclusion-body myositis muscle.Proceedings of the National Academy of Sciences of the United States of America · 2006
   Article
7. Amyloid beta(1-42) peptide alters the gating of human and mouse alpha-bungarotoxin-sensitive nicotinic receptors.The Journal of physiology · 2003
   Article
8. Newest pathogenetic considerations in inclusion-body myositis: possible role of amyloid-beta, cholesterol, relation to aging and to Alzheimer's disease.Current rheumatology reports · 2002
   Review
9. Accumulation of amyloid-beta protein in exocrine glands of transgenic mice overexpressing a carboxyl terminal portion of amyloid protein precursor.International journal of experimental pathology · 2000
   Article

Corrections and comments

• Comment on
  Transgenic mice over-expressing the C-99 fragment of betaPP with an alpha-secretase site mutation develop a myopathy similar to human inclusion body myositis.1998
• Comment on
  Amyloid-beta deposition in skeletal muscle of transgenic mice: possible model of inclusion body myopathy.1998

Authors and funding

2 authors.

Funding

No grant is acknowledged in the PubMed record.

Abstract

PubMed holds no abstract for this paper.

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