ReviewThe Journal of clinical psychiatry2006
Genetics, transcriptomics, and proteomics of Alzheimer's disease.
Review in The Journal of clinical psychiatry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 106 citations in OpenAlex.
- The Hippo signaling pathway as a therapeutic target in Alzheimer's disease.Molecular neurodegeneration · 2025Review
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- Exploratory Longitudinal Study of Ocular Structural and Visual Functional Changes in Subjects at High Genetic Risk of Developing Alzheimer's Disease.Biomedicines · 2023Article
- Screening for Genetic Mutations Associated with Early-Onset Alzheimer's Disease in Han Chinese.Current Alzheimer research · 2022Article
- Review
- Utility of Animal Models to Understand Human Alzheimer's Disease, Using the Mastermind Research Approach to Avoid Unnecessary Further Sacrifices of Animals.International journal of molecular sciences · 2020Review
- Plasma Biomarkers: Potent Screeners of Alzheimer's Disease.American journal of Alzheimer's disease and other dementias · 2019Review
- Inferring disease risk genes from sequencing data in multiplex pedigrees through sharing of rare variants.Genetic epidemiology · 2019Article
- Extracellular matrix proteomics in schizophrenia and Alzheimer's disease.Analytical and bioanalytical chemistry · 2017Review
- Alzheimer's disease: are blood and brain markers related? A systematic review.Annals of clinical and translational neurology · 2016Article
- Mutation-based structural modification and dynamics study of amyloid beta peptide (1-42): An in-silico-based analysis to cognize the mechanism of aggregation.Genomics data · 2016Article
- Neurodegeneration and Alzheimer's disease (AD). What Can Proteomics Tell Us About the Alzheimer's Brain?Molecular & cellular proteomics : MCP · 2016Review
- Analysis of Differentially Expressed Genes Associated With Alzheimer's Disease Based on Bioinformatics Methods.American journal of Alzheimer's disease and other dementias · 2015Article
- Label-free quantitative LC-MS proteomics of Alzheimer's disease and normally aged human brains.Journal of proteome research · 2012Article
- Gene expression reveals overlap between normal aging and Alzheimer's disease genes.Neurobiology of aging · 2011Article
- Association between GAB2 haplotype and higher glucose metabolism in Alzheimer's disease-affected brain regions in cognitively normal APOEε4 carriers.NeuroImage · 2011Article
- Article
- Identifying genetic interactions in genome-wide data using Bayesian networks.Genetic epidemiology · 2010Article
- Quantitative proteomic analysis of mitochondria in aging PS-1 transgenic mice.Cellular and molecular neurobiology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
objectiveTo provide an updated overview of the methods used in genetic, transcriptomic, and proteomic studies in Alzheimer's disease and to demonstrate the importance of those methods for the improvement of the current diagnostic and therapeutic possibilities. DATA SOURCES: MEDLINE-based search of 233 peer-reviewed articles published between 1975 and 2006. DATA SYNTHESIS: Alzheimer's disease is a genetically heterogeneous disorder. Rare mutations in the amyloid precursor protein, presenilin 1, and presenilin 2 genes have shown the importance of the amyloid metabolism for its development. In addition, converging evidence from population-based genetic studies, gene expression studies, and protein profile studies in the brain and in the cerebrospinal fluid suggest the existence of several pathogenetic pathways such as amyloid precursor protein processing, beta-amyloid degradation, tau phosphorylation, proteolysis, protein misfolding, neuroinflammation, oxidative stress, and lipid metabolism.
conclusionsThe development of high-throughput genotyping methods and of elaborated statistical analyses will contribute to the identification of genetic risk profiles related to the development and course of this devastating disease. The integration of knowledge derived from genetic, transcriptomic, and proteomic studies will greatly advance our understanding of the causes of Alzheimer's disease, improve our capability of establishing an early diagnosis, help define disease subgroups, and ultimately help to pave the road toward improved and tailored treatments.
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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.