ArticleAMIA Joint Summits on Translational Science proceedings. AMIA Joint Summits on Translational Science2014
Automatic gene prioritization in support of the inflammatory contribution to Alzheimer's disease.
Article in AMIA Joint Summits on Translational Science proceedings. AMIA Joint Summits on Translational Science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Sufentanil attenuates inflammation and oxidative stress in sepsis-induced acute lung injury by downregulating KNG1 expression.Molecular medicine reports · 2020Article
- Celastrol Alleviates Chronic Obstructive Pulmonary Disease by Inhibiting Cellular Inflammation Induced by Cigarette Smoke via the Ednrb/Kng1 Signaling Pathway.Frontiers in pharmacology · 2018Article
- Mining the literature for genes associated with placenta-mediated maternal diseases.AMIA ... Annual Symposium proceedings. AMIA Symposium · 2017Article
- Article
- Identification of cerebrospinal fluid pharmacodynamic biomarkers and molecular correlates of brain activity in a Phase 2 clinical trial of the Alzheimer's disease drug candidate CT1812.Alzheimer's & dementia (New York, N. Y.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
This research seeks to extend the process of novel therapeutic gene target discovery for the treatment of Alzheimer's disease (AD). Gene-gene and gene-pathway annotation tools as well as human analysis are used to explore likely connections between potential gene targets and biochemical mechanisms of AD and associated genes. Rule-based annotation systems, such as GeneRanker, can be applied to the continuously growing volume of literature to extract relevant gene lists. The subsequent challenge is to abstract biological significance from associated genes to aid in discovery of novel therapeutic gene targets. Automatic annotation of genes deemed significant by data-driven assays and knowledge-driven analysis is limited. Therefore, human analysis is still crucial to exploring novel gene targets and new disease models. This research illustrates a method of analysis of an extracted gene list which lead to the discovery of KNG1 as a possible therapeutic target, suggests a connection between inflammation and AD pathogenesis.
Identifiers
25717399PMC4333706W110722971What 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.