ArticleThe American journal of pathology2005
Up-regulation of inhibitors of protein phosphatase-2A in Alzheimer's disease.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
102 citing papers in PubMed, 2 syntheses or guidelines pooled it, 219 citations in OpenAlex.
- C/EBPβ: A transcription factor associated with the irreversible progression of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Pooled it
- Similarities and Differences in the Pattern of Tau Hyperphosphorylation in Physiological and Pathological Conditions: Impacts on the Elaboration of Therapies to Prevent Tau Pathology.Frontiers in neurology · 2020Pooled it
- Hexaraphane as a potential therapeutic strategy for tauopathies.Redox biology · 2026Article
- Implications of virus-induced stress granules in tauopathies.Translational neurodegeneration · 2026Review
- Protein phosphatase 2A (PP2A) function in male germ cells and its importance for male fertility.Endocrine connections · 2025Review
- Biomarkers and Target-Specific Small-Molecule Drugs in Alzheimer's Diagnostic and Therapeutic Research: From Amyloidosis to Tauopathy.Neurochemical research · 2024Review
- H3K4 Trimethylation Mediate Hyperhomocysteinemia Induced Neurodegeneration via Suppressing Histone Acetylation by ANP32A.Molecular neurobiology · 2024Article
- Research Progress on the Pathogenesis, Diagnosis, and Drug Therapy of Alzheimer's Disease.Brain sciences · 2024Review
- Visualization Analysis of Tau Protein in the Brain of Alzheimer's Disease: A Scoping Literature Review.Current Alzheimer research · 2024Article
- Does modulation of tau hyperphosphorylation represent a reasonable therapeutic strategy for Alzheimer's disease? From preclinical studies to the clinical trials.Molecular psychiatry · 2023Review
- Benzodiazepines in Alzheimer's disease: beneficial or detrimental effects.Inflammopharmacology · 2023Review
- Promising Molecular Targets in Pharmacological Therapy for Neuronal Damage in Brain Injury.Antioxidants (Basel, Switzerland) · 2023Review
- Proposed mechanisms of tau: relationships to traumatic brain injury, Alzheimer's disease, and epilepsy.Frontiers in neurology · 2023Article
- Emerging evidence for dysregulated proteome cargoes of tau-propagating extracellular vesicles driven by familial mutations of tau and presenilin.Extracellular vesicles and circulating nucleic acids · 2023Article
- Thirty years of SET/TAF1β/I2PP2A: from the identification of the biological functions to its implications in cancer and Alzheimer's disease.Bioscience reports · 2022Review
- A Review of the Recent Advances in Alzheimer's Disease Research and the Utilization of Network Biology Approaches for Prioritizing Diagnostics and Therapeutics.Diagnostics (Basel, Switzerland) · 2022Review
- A bidirectional switch in the Shank3 phosphorylation state biases synapses toward up- or downscaling.eLife · 2022Article
- Cross Talk between α7 and α3β4 Nicotinic Receptors Prevents Their Desensitization in Human Chromaffin Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- CK2 and protein kinases of the CK1 superfamily as targets for neurodegenerative disorders.Frontiers in molecular biosciences · 2022Review
- Alzheimer's Disease: A Molecular View of β-Amyloid Induced Morbific Events.Biomedicines · 2021Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The activity of protein phosphatase-2A (PP2A) is compromised and is believed to be a cause of the abnormal hyperphosphorylation of tau in Alzheimer's disease (AD) brain. We investigated in AD the role of the two known endogenous PP2A inhibitors, called I1(PP2A) and I2(PP2A), which regulate the intracellular activity of PP2A in mammalian tissues. We found a significant increase in the neocortical levels of I1(PP2A) and I2(PP2A) in AD as compared to control cases by in situ hybridization. The immunohistochemical studies revealed that I2(PP2A) was translocated from neuronal nuclei to cytoplasm in AD. The 39-kd full-length I2(PP2A) was selectively cleaved into an approximately 20-kd fragment in AD brain cytosol. Digestion of the recombinant human I2(PP2A) with AD brain extract showed an increase in the generation of the approximately 20 kd and other fragments of the inhibitor as compared to control brain extract. Double-immunohistochemical studies revealed co-localization of PP2A with PP2A inhibitors in neuronal cytoplasm and co-localization of the inhibitors with abnormally hyperphosphorylated tau. These studies suggest the possible involvement of I1(PP2A) and I2(PP2A) in the abnormal hyperphosphorylation of tau in AD.
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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.