ReviewHistology and histopathology2005
Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury.
Review in Histology and histopathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 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
113 citing papers in PubMed, 184 citations in OpenAlex.
- Sex differences in the effects of chronic stress and oxycodone associative learning on glial markers in rat hippocampus.Neuroscience · 2026Article
- High protein ingestion does not affect whole-body insulin sensitivity in individuals with overweight or obesity.Journal of the Endocrine Society · 2026Article
- Molecular Networks of Redox Dysregulation in Fetal Alcohol Spectrum Disorders: Mechanisms and Therapeutic Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Genetic correlation analysis of Alzheimer's disease and stroke implicates PHLPP1 as a shared locus in individuals of African ancestry.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Local genetic correlation analysis of Alzheimer's disease and stroke implicatesmedRxiv : the preprint server for health sciences · 2025Article
- Downregulation of AKT-mediated p27IBRO neuroscience reports · 2025Article
- Development of a Human Preclinical Platform for the Identification of Neuroprotective Compounds.The European journal of neuroscience · 2025Article
- Dapagliflozin Ameliorates Doxorubicin-Induced Chemobrain and Cognitive Abnormalities in Rats: Modulation of AKT/GSK-3β and Wnt/β-Catenin Pathways.Neurochemical research · 2025Article
- Dual Impact of Iron Deficiency and Antibiotics on Host Metabolism: A Tissue-Level Analysis.Metabolites · 2025Article
- Time restricted feeding with or without ketosis influences metabolism-related gene expression in a tissue-specific manner in aged rats.GeroScience · 2025Article
- Alterations in Striatal Architecture and Biochemical Markers' Levels During Postnatal Development in the Rat Model of an Attention Deficit/Hyperactivity Disorder (ADHD).International journal of molecular sciences · 2024Article
- Time restricted feeding with or without ketosis influences metabolism-related gene expression in a tissue-specific manner in aged rats.bioRxiv : the preprint server for biology · 2024Article
- Maternal gut Bifidobacterium breve modifies fetal brain metabolism in germ-free mice.Molecular metabolism · 2024Article
- Vagus nerve stimulation: a physical therapy with promising potential for central nervous system disorders.Frontiers in neurology · 2024Review
- Rett and Rett-related disorders: Common mechanisms for shared symptoms?Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Article
- Addressing Peroxisome Proliferator-Activated Receptor-gamma in 3-Nitropropionic Acid-Induced Striatal Neurotoxicity in Rats.Molecular neurobiology · 2022Article
- Unravelling the potential neuroprotective facets of erythropoietin for the treatment of Alzheimer's disease.Metabolic brain disease · 2022Review
- Neuroprotective and antioxidative effects of pioglitazone in brain tissue adjacent to the ischemic core are mediated by PI3K/Akt and Nrf2/ARE pathways.Journal of molecular medicine (Berlin, Germany) · 2021Article
- IGF1R Deficiency Modulates Brain Signaling Pathways and Disturbs Mitochondria and Redox Homeostasis.Biomedicines · 2021Article
53 more citing papers are in PubMed but not listed here.
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
Protein kinase B, also known as Akt, is a serine/threonine kinase and plays a critical role in the modulation of cell development, growth, and survival. Interestingly, Akt is ubiquitously expressed throughout the body, but its expression in the nervous system is substantially up-regulated during cellular stress, suggesting a more expansive role for Akt in the nervous system that may involve cellular protection. In this regard, a body of recent work has identified a robust capacity for Akt and its downstream substrates to foster both neuronal and vascular survival during apoptotic injury. Cell survival by Akt is driven by the modulation of both intrinsic cellular pathways that oversee genomic DNA integrity and extrinsic mechanisms that control inflammatory microglial activation. A series of distinct pathways are regulated by Akt that include the Forkhead family of transcription factors, GSK-3 beta, beta-catenin, c-Jun, CREB, Bad, IKK, and p53. Culminating below these substrates of Akt are the control of caspase mediated pathways that promote genomic integrity as well as prevent inflammatory cell demise. With further levels of progress in defining the cellular role of Akt, the attractiveness of Akt as a vital and broad cytoprotectant for both neuronal and vascular cell populations should continue to escalate.
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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.