ReviewFrontiers in cellular neuroscience2015
Compensatory mechanisms in genetic models of neurodegeneration: are the mice better than humans?
Review in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
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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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Transcriptional signatures of brain aging and Alzheimer's disease: What are our rodent models telling us?Behavioural brain research · 2017Pooled it
- Single-dose administration of therapeutic divalent siRNA targeting MECP2 prevents lethality in an MECP2 duplication mouse model.Nature communications · 2026Article
- Single-nucleus transcriptomics of an engineered pig model reveals microglia-T cell interactions driving Huntington's disease neurodegeneration.Nature biomedical engineering · 2026Article
- What can the common fruit fly teach us about stroke?: lessons learned from the hypoxic tolerantFrontiers in cellular neuroscience · 2024Review
- Constitutive depletion of brain serotonin differentially affects rats' social and cognitive abilities.iScience · 2023Article
- Therapeutic Effect of IL-21 Blockage by Gene Therapy in Experimental Autoimmune Encephalomyelitis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Article
- Organ-on-a-chip technologies to study neuromuscular disorders: possibilities, limitations, and future hopes.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2021Article
- Parkin regulates drug-taking behavior in rat model of methamphetamine use disorder.Translational psychiatry · 2021Article
- Article
- Neural compensation in presymptomatic hAPP mouse models of Alzheimer's disease.Learning & memory (Cold Spring Harbor, N.Y.) · 2020Review
- Transgenic Mice Overexpressing HumanInternational journal of molecular sciences · 2020Article
- Article
- Are we listening to everything the PARK genes are telling us?The Journal of comparative neurology · 2019Review
- Dynamic interplay between H-current and M-current controls motoneuron hyperexcitability in amyotrophic lateral sclerosis.Cell death & disease · 2019Article
- Evaluation of the Neuroprotective Effect of Sirt3 in Experimental Stroke.Translational stroke research · 2019Article
- Vrk1 partial Knockdown in Mice Results in Reduced Brain Weight and Mild Motor Dysfunction, and Indicates Neuronal VRK1 Target Pathways.Scientific reports · 2018Article
- Nucleoside diphosphate kinase B regulates angiogenic responses in the endothelium via caveolae formation and c-Src-mediated caveolin-1 phosphorylation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Cx47 fine-tunes the handling of serum lipids but is dispensable for lymphatic vascular function.PloS one · 2017Article
- 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegenerative diseases are one of the main causes of mental and physical disabilities. Neurodegeneration has been estimated to begin many years before the first clinical symptoms manifest, and even a prompt diagnosis at this stage provides very little advantage for a more effective treatment as the currently available pharmacotherapies are based on disease symptomatology. The etiology of the majority of neurodegenerative diseases remains unknown, and even for those diseases caused by identified genetic mutations, the direct pathways from gene alteration to final cell death have not yet been fully elucidated. Advancements in genetic engineering have provided many transgenic mice that are used as an alternative to pharmacological models of neurodegenerative diseases. Surprisingly, even the models reiterating the same causative mutations do not fully recapitulate the inevitable neuronal loss, and some fail to even show phenotypic alterations, which suggests the possible existence of compensatory mechanisms. A better evaluation of these mechanisms may not only help us to explain why neurodegenerative diseases are mostly late-onset disorders in humans but may also provide new markers and targets for novel strategies designed to extend neuronal function and survival. The aim of this mini-review is to draw attention to this under-explored field in which investigations may reasonably contribute to unveiling hidden reserves in the organism.
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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.