Evidence map›Paper›PMID 16809372›Full record

ReviewThe Journal of physiology2006

Physiological roles for amyloid beta peptides.

Hugh A Pearson, Chris Peers

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 5% 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

120 citing papers in PubMed, 2 syntheses or guidelines pooled it, 284 citations in OpenAlex.

  1. The Role of c-Abl in Alzheimer's Disease: Guilty or not Guilty?Cellular and molecular neurobiology · 2025
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60 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

2 authors at 1 institution in 1 country.

Hugh A PearsonFaculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK. h.a.pearson@leeds.ac.uk
Chris Peers
University of Leeds · GB

Funding

Medical Research Council G0600936Wellcome Trust
6 · The paper itself

Abstract

Alzheimer's disease is recognized post mortem by the presence of extracellular senile plaques, made primarily of aggregation of amyloid beta peptide (Abeta). This peptide has consequently been regarded as the principal toxic factor in the neurodegeneration of Alzheimer's disease. As such, intense research effort has been directed at determining its source, activity and fate, primarily with a view to preventing its formation or its biological activity, or promoting its degradation. Clearly, much progress has been made concerning its formation by proteolytic processing of the amyloid precursor protein, and its degradation by enzymes such as neprilysin and insulin degrading enzyme. The activities of Abeta, however, are numerous and yet to be fully elucidated. What is currently emerging from such studies is a diffuse but steadily growing body of data that suggests Abeta has important physiological functions and, further, that it should only be regarded as toxic when its production and degradation are imbalanced. Here, we review these data and suggest that physiological levels of Abeta have important physiological roles, and may even be crucial for neuronal cell survival. Thus, the view of Abeta being a purely toxic peptide requires re-evaluation.

Indexed as

Protein Processing, Post-TranslationalAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsCalcium Channels, L-TypeCell SurvivalCentral Nervous SystemHumansHypoxiaNeuronsPotassium ChannelsSynaptic TransmissionAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCalcium Channels, L-TypePotassium Channels

Identifiers

PMID16809372
PMCPMC1819417
OpenAlexW1536538075

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.