Evidence map›Paper›PMID 17659362›Full record

ReviewHuman genetics2007

Progress in defining the molecular biology of age related macular degeneration.

Andrew Lotery, Dorothy Trump

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
9.4field-weighted citation impact, top 2% 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

23 citing papers in PubMed, 71 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

2 authors at 2 institutions in 1 country.

Andrew LoteryClinical Neurosciences Division, University of Southampton, Southampton General Hospital, Southampton, SO16 6YD, UK. a.j.lotery@soton.ac.uk
Dorothy Trump
University of Manchester · GBUniversity of Southampton · GB

Funding

Wellcome Trust 076169
6 · The paper itself

Abstract

Age related macular degeneration (AMD) is an extremely prevalent complex genetic disorder. Its incidence rises exponentially in the elderly to a frequency of 1 in 2 in the general population by age 85. It affects approximately 25 million people and is the commonest cause of irreversible visual loss in the Western world. It is therefore a major public health problem. However, until recently its aetiology was unknown. Our understanding of both the molecular biology of AMD and the relevant clinical treatments has progressed dramatically in the last 2 years. Two genes of large effect have been identified which together contribute to over 70% of the population attributable risk of AMD. Treatments which inhibit expression of vascular endothelial growth factor have been developed which can rescue vision in the "wet" form of the disease. The association of complement factor H with AMD highlights the importance of the alternative complement pathway in the development of AMD whilst the pathophysiology of the serine protease HTRA1 is now under intensive study. This review will give an insight into these developments and will summarise our current knowledge of the molecular biology of AMD.

Indexed as

AgedAnimalsATP-Binding Cassette TransportersChromosomes, Human, Pair 10Complement Factor BComplement Factor HDisease Models, AnimalExtracellular Matrix ProteinsHumansMacular DegenerationMolecular BiologyMutationPhenotypeRetinal DrusenRisk FactorsVascular Endothelial Growth Factor AABCA4 protein, humanATP-Binding Cassette TransportersComplement Factor BComplement Factor HEFEMP1 protein, humanExtracellular Matrix ProteinsVascular Endothelial Growth Factor A

Identifiers

PMID17659362
OpenAlexW2159999364

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.