ReviewProgress in neurobiology2008
The injured nervous system: a Darwinian perspective.
Review in Progress in neurobiology, 2008. 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, 62 citations in OpenAlex.
- Review
- Adult neurogenesis and "immature" neurons in mammals: an evolutionary trade-off in plasticity?Brain structure & function · 2024Review
- Editorial: ATF3: a crucial stress-responsive gene of glia and neurons in CNS.Frontiers in molecular neuroscience · 2024Article
- Neurotrophic Factors as Regenerative Therapy for Neurodegenerative Diseases: Current Status, Challenges and Future Perspectives.International journal of molecular sciences · 2023Review
- Knowledge gaps in Alzheimer's disease immune biomarker research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Review
- Brain Plasticity in Humans and Model Systems: Advances, Challenges, and Future Directions.International journal of molecular sciences · 2021Review
- Amazon rainforest rodents (Proechimys) are resistant to post-stroke epilepsy.Scientific reports · 2021Article
- The mTORC1/eIF4E/HIF-1α Pathway Mediates Glycolysis to Support Brain Hypoxia Resistance in the Gansu Zokor,Frontiers in physiology · 2021Article
- Evaluation of M2-like macrophage enrichment after diffuse traumatic brain injury through transient interleukin-4 expression from engineered mesenchymal stromal cells.Journal of neuroinflammation · 2020Article
- Potential of Chitosan and Its Derivatives for Biomedical Applications in the Central Nervous System.Frontiers in bioengineering and biotechnology · 2020Review
- Thyroid Hormone and Neural Stem Cells: Repair Potential Following Brain and Spinal Cord Injury.Frontiers in neuroscience · 2020Review
- Brain Structural Plasticity: From Adult Neurogenesis to Immature Neurons.Frontiers in neuroscience · 2020Review
- Microglial subtypes: diversity within the microglial community.The EMBO journal · 2019Review
- A review of the alleged health hazards of monosodium glutamate.Comprehensive reviews in food science and food safety · 2019Article
- Nanomaterial-Based Approaches for Neural Regeneration.Pharmaceutics · 2019Review
- Newly Generated and Non-Newly Generated "Immature" Neurons in the Mammalian Brain: A Possible Reservoir of Young Cells to Prevent Brain Aging and Disease?Journal of clinical medicine · 2019Review
- Humans and Dolphins: Decline and Fall of Adult Neurogenesis.Frontiers in neuroscience · 2018Review
- Brain Plasticity in Mammals: An Example for the Role of Comparative Medicine in the Neurosciences.Frontiers in veterinary science · 2018Article
- Protective effects of curcumin against rotenone-induced rat model of Parkinson's disease: in vivo electrophysiological and behavioral study.Metabolic brain disease · 2017Article
- Seasonal and post-trauma remodeling in cone-dominant ground squirrel retina.Experimental eye research · 2016Review
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
Much of the permanent damage that occurs in response to nervous system damage (trauma, infection, ischemia, etc.) is mediated by endogenous secondary processes that can contribute to cell death and tissue damage (excitotoxicity, oxidative damage and inflammation). For humans to evolve mechanisms to minimize secondary pathophysiological events following CNS injuries, selection must occur for individuals who survive such insults. Two major factors limit the selection for beneficial responses to CNS insults: for many CNS disease states the principal risk factor is advanced, post-reproductive age and virtually all severe CNS traumas are fatal in the absence of modern medical intervention. An alternative hypothesis for the persistence of apparently maladaptive responses to CNS damage is that the secondary exacerbation of damage is the result of unavoidable evolutionary constraints. That is, the nervous system could not function under normal conditions if the mechanisms that caused secondary damage (e.g., excitotoxicity) in response to injury were decreased or eliminated. However, some vertebrate species normally inhabit environments (e.g., hypoxia in underground burrows) that could potentially damage their nervous systems. Yet, neuroprotective mechanisms have evolved in these animals indicating that natural selection can occur for traits that protect animals from nervous system damage. Many of the secondary processes and regeneration-inhibitory factors that exacerbate injuries likely persist because they have been adaptive over evolutionary time in the healthy nervous system. Therefore, it remains important that researchers consider the role of the processes in the healthy or developing nervous system to understand how they become dysregulated following injury.
Indexed as
Identifiers
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.