ReviewContinuum (Minneapolis, Minn.)2013
New genes and new insights from old genes: update on Alzheimer disease.
Review in Continuum (Minneapolis, Minn.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled 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.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Cerebral changes improved by physical activity during cognitive decline: A systematic review on MRI studies.NeuroImage. Clinical · 2019Pooled it
- Biologics as Therapeutical Agents Under Perspective Clinical Studies for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2025Review
- Apolipoprotein E and Alzheimer's Disease in Italian Population: Systematic Review and Meta-Analysis.Brain sciences · 2024Review
- Pharmacogenomics for neurodegenerative disorders - a focused review.Frontiers in pharmacology · 2024Review
- Assessment of Neurodegenerative Changes in Turkeys Fed Diets with Different Proportions of Arginine and Methionine Relative to Lysine.Animals : an open access journal from MDPI · 2022Article
- Identification of miRNA-mediated gene regulatory networks in L-methionine exposure counteracts cocaine-conditioned place preference in mice.Frontiers in genetics · 2022Article
- Article
- Candidate l-methionine target piRNA regulatory networks analysis response to cocaine-conditioned place preference in mice.Brain and behavior · 2021Article
- Methionine Diet Evoked Hyperhomocysteinemia Causes Hippocampal Alterations, Metabolomics Plasma Changes and Behavioral Pattern in Wild Type Rats.International journal of molecular sciences · 2021Article
- Public Willingness to Undergo Presymptomatic Genetic Testing for Alzheimer's Disease.Neurology research international · 2019Article
- Genomic approaches to the assessment of human spina bifida risk.Birth defects research · 2017Review
- Is L-methionine a trigger factor for Alzheimer's-like neurodegeneration?: Changes in Aβ oligomers, tau phosphorylation, synaptic proteins, Wnt signaling and behavioral impairment in wild-type mice.Molecular neurodegeneration · 2015Article
- Gene hunting in autism spectrum disorder: on the path to precision medicine.The Lancet. Neurology · 2015Review
- Increased Transcript Complexity in Genes Associated with Chronic Obstructive Pulmonary Disease.PloS one · 2015Article
- Genetic heterogeneity in Alzheimer disease and implications for treatment strategies.Current neurology and neuroscience reports · 2014Review
- Rare Variants and Transcriptomics in Alzheimer disease.Current genetic medicine reports · 2014Article
- Immunotherapy for Alzheimer's disease.Biochemical pharmacology · 2014Review
- Combotherapy and current concepts as well as future strategies for the treatment of Alzheimer's disease.Neuropsychiatric disease and treatment · 2014Review
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.
Funding
Abstract
purpose of reviewThis article discusses the current status of knowledge regarding the genetic basis of Alzheimer disease (AD) with a focus on clinically relevant aspects. RECENT
findingsThe genetic architecture of AD is complex, as it includes multiple susceptibility genes and likely nongenetic factors. Rare but highly penetrant autosomal dominant mutations explain a small minority of the cases but have allowed tremendous advances in understanding disease pathogenesis. The identification of a strong genetic risk factor, APOE, reshaped the field and introduced the notion of genetic risk for AD. More recently, large-scale genome-wide association studies are adding to the picture a number of common variants with very small effect sizes. Large-scale resequencing studies are expected to identify additional risk factors, including rare susceptibility variants and structural variation. SUMMARY: Genetic assessment is currently of limited utility in clinical practice because of the low frequency (Mendelian mutations) or small effect size (common risk factors) of the currently known susceptibility genes. However, genetic studies are identifying with confidence a number of novel risk genes, and this will further our understanding of disease biology and possibly the identification of therapeutic targets.
Indexed as
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What OpenQuestion holds
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.