ReviewCurrent neurology and neuroscience reports2001
Of replications and refutations: the status of Alzheimer's disease genetic research.
Review in Current neurology and neuroscience reports, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed, 33 citations in OpenAlex.
- Autophagy-lysosomal pathway impairment and cathepsin dysregulation in Alzheimer's disease.Frontiers in molecular biosciences · 2024Review
- Alzheimer's genetics in the GWAS era: a continuing story of 'replications and refutations'.Current neurology and neuroscience reports · 2011Review
- Clinic visits and prescribing patterns among Veterans Affairs Maryland Health Care System dementia patients.The journal of nutrition, health & aging · 2010Article
- Upregulation of CRABP1 in human neuroblastoma cells overproducing the Alzheimer-typical Abeta42 reduces their differentiation potential.BMC medicine · 2008Article
- Lens defects and age-related fiber cell degeneration in a mouse model of increased AbetaPP gene dosage in Down syndrome.The American journal of pathology · 2002Article
- Dancing in the dark? The status of late-onset Alzheimer's disease genetics.Journal of molecular neuroscience : MN · 2001Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a genetically complex and heterogeneous disorder. To date, mutations in three genes (APP, PSEN1, PSEN2) have been described to cause familial early-onset AD. In addition, a common polymorphism in the gene encoding apolipoprotein E (APOE) has been associated with the more common late-onset form of the disease. However, many studies have shown that genetic factors other than APOE play an important role in late-onset AD. Along these lines, a recent report predicted the existence of at least four additional late-onset AD genes, one of which was estimated to have a much greater contribution to age of onset variation than the APOE epsilon 4-allele. However, most of the nearly three dozen loci that have been proposed as putative AD genes to date have been followed by both replications and refutations, making consensus impossible. In this overview, we discuss the current status of genetic research in AD, including a brief summary of applicable analytic tools, and a summary of recent findings suggesting the existence of novel AD genes on chromosomes 10, 11, and 12.
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Registered trials
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.