ReviewExperimental neurology2021
Genes causing congenital hydrocephalus: Their chromosomal characteristics of telomere proximity and DNA compositions.
Review in Experimental neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- NFκB1: a common biomarker linking Alzheimer's and Parkinson's disease pathology.Frontiers in neuroscience · 2025Article
- Molecular signatures of normal pressure hydrocephalus: a large-scale proteomic analysis of cerebrospinal fluid.Fluids and barriers of the CNS · 2024Article
- The impact of telomere length on the risk of idiopathic normal pressure hydrocephalus: a bidirectional Mendelian randomization study.Scientific reports · 2024Article
- Reduced GLP-1R availability in the caudate nucleus with Alzheimer's disease.Frontiers in aging neuroscience · 2024Article
- A Carboxy-terminal Smarcb1 Point Mutation Induces Hydrocephalus Formation and Affects AP-1 and Neuronal Signalling Pathways in Mice.Cellular and molecular neurobiology · 2023Article
- X-linked hydrocephalus genes: Their proximity to telomeres and high A + T content compared to Parkinson's disease.Experimental neurology · 2023Review
- Sleep Disturbance and Severe Hydrocephalus in a Normally Behaving Wistar Rat With Traumatic Brain Injury.Neurotrauma reports · 2023Article
- Mutability of druggable kinases and pro-inflammatory cytokines by their proximity to telomeres and A+T content.PloS one · 2023Article
- Activation Mechanism of RhoA Caused by Constitutively Activating Mutations G14V and Q63L.International journal of molecular sciences · 2022Article
- Long-term recovery behavior of brain tissue in hydrocephalus patients after shunting.Communications biology · 2022Article
- Prenatal diagnosis of Walker-Warburg syndrome due to compound mutations in the B3GALNT2 gene.The journal of gene medicine · 2022Article
- Drug-Targeted Genomes: Mutability of Ion Channels and GPCRs.Biomedicines · 2022Article
- Article
- TRPV4 mRNA is elevated in the caudate nucleus with NPH but not in Alzheimer's disease.Frontiers in genetics · 2022Article
- Review
- Factors Associated with Mutations: Their Matching Rates to Cardiovascular and Neurological Diseases.International journal of molecular sciences · 2021Article
- Boundary conditions investigation to improve computer simulation of cerebrospinal fluid dynamics in hydrocephalus patients.Communications biology · 2021Article
- Molecular Mechanisms and Risk Factors for the Pathogenesis of Hydrocephalus.Frontiers in genetics · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Congenital hydrocephalus (CH) is caused by genetic mutations, but whether factors impacting human genetic mutations are disease-specific remains elusive. Given two factors associated with high mutation rates, we reviewed how many disease-susceptible genes match with (i) proximity to telomeres or (ii) high adenine and thymine (A + T) content in human CH as compared to other disorders of the central nervous system (CNS). We extracted genomic information using a genome data viewer. Importantly, 98 of 108 genes causing CH satisfied (i) or (ii), resulting in >90% matching rate. However, such a high accordance no longer sustained as we checked two factors in Alzheimer's disease (AD) and/or familial Parkinson's disease (fPD), resulting in 84% and 59% matching, respectively. A disease-specific matching of telomere proximity or high A + T content predicts causative genes of CH much better than neurodegenerative diseases and other CNS conditions, likely due to sufficient number of known causative genes (n = 108) and precise determination and classification of the genotype and phenotype. Our analysis suggests a need for identifying genetic basis of both factors before human clinical studies, to prioritize putative genes found in preclinical models into the likely (meeting at least one) and more likely candidate (meeting both), which predisposes human genes to mutations.
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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.