ReviewProgress in molecular biology and translational science2012
Protein phosphatases and Alzheimer's disease.
Review in Progress in molecular biology and translational science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Genetic determinants of common epilepsies: a meta-analysis of genome-wide association studies.The Lancet. Neurology · 2014Pooled it
- Neuroprotective Mechanisms of Ficus deltoidea in an Alzheimer's Disease-Like Rat Model: Targeting Tau Hyperphosphorylation Through Glycogen Synthase Kinase-3 Beta and Protein Phosphatase 2A Regulation.Neurochemical research · 2026Article
- The clinical missense variant E282K in PPP3CA/calcineurin shifts substrate dephosphorylation by altering active site recruitment.Nature communications · 2026Article
- Allele-specific alternative polyadenylation links noncoding genetic variation to Alzheimer's disease risk.bioRxiv : the preprint server for biology · 2026Article
- Pathological Calcium Signaling in Traumatic Brain Injury and Alzheimer's Disease: From Acute Neuronal Injury to Chronic Neurodegeneration.International journal of molecular sciences · 2025Review
- Evaluation of altered cell-cell communication between glia and neurons in the hippocampus of 3xTg-AD mice at two time points.Journal of cell communication and signaling · 2025Article
- Unraveling APOE4's Role in Alzheimer's Disease: Pathologies and Therapeutic Strategies.Current protein & peptide science · 2025Review
- Evaluation of altered cell-cell communication between glia and neurons in the hippocampus of 3xTg-AD mice at two time points.bioRxiv : the preprint server for biology · 2024Article
- Molecular Role of Protein Phosphatases in Alzheimer's and Other Neurodegenerative Diseases.Biomedicines · 2024Review
- Exosomal Dynamics and Brain Redox Imbalance: Implications in Alzheimer's Disease Pathology and Diagnosis.Antioxidants (Basel, Switzerland) · 2024Review
- Untangling Tau: Molecular Insights into Neuroinflammation, Pathophysiology, and Emerging Immunotherapies.Current issues in molecular biology · 2023Review
- Role of Non-Receptor-Type Tyrosine Phosphatases in Brain-Related Diseases.Molecular neurobiology · 2023Review
- Exploring the role of COX-2 in Alzheimer's disease: Potential therapeutic implications of COX-2 inhibitors.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Review
- Exploratory genome-wide analyses of cortical inhibition, facilitation, and plasticity in late-life depression.Translational psychiatry · 2023Article
- Unravelling the mechanotransduction pathways in Alzheimer's disease.Journal of biological engineering · 2023Review
- The Breakthroughs and Caveats of Using Human Pluripotent Stem Cells in Modeling Alzheimer's Disease.Cells · 2023Review
- Behavioral and Proteomic Studies Reveal Methylglyoxal Activate Pathways Associated with Alzheimer's Disease.ACS pharmacology & translational science · 2023Article
- Multi-omic integration via similarity network fusion to detect molecular subtypes of ageing.Brain communications · 2023Article
- Nuclear Inhibitor of Protein Phosphatase 1 (NIPP1) Regulates CNS Tau Phosphorylation and Myelination During Development.Molecular neurobiology · 2022Article
- The accumulation of copper in the brain of Down syndrome promotes oxidative stress: possible mechanism underlying cognitive impairment.Journal of clinical biochemistry and nutrition · 2022Article
7 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
4 authors at 3 institutions in 1 country.
Funding
Abstract
Alzheimer's Disease (AD) is characterized by progressive loss of cognitive function, linked to marked neuronal loss. Pathological hallmarks of the disease are the accumulation of the amyloid-β (Aβ) peptide in the form of amyloid plaques and the intracellular formation of neurofibrillary tangles (NFTs). Accumulating evidence supports a key role for protein phosphorylation in both the normal and pathological actions of Aβ as well as the formation of NFTs. NFTs contain hyperphosphorylated forms of the microtubule-binding protein tau, and phosphorylation of tau by several different kinases leads to its aggregation. The protein kinases involved in the generation and/or actions of tau or Aβ are viable drug targets to prevent or alleviate AD pathology. However, it has also been recognized that the protein phosphatases that reverse the actions of these protein kinases are equally important. Here, we review recent advances in our understanding of serine/threonine and tyrosine protein phosphatases in the pathology of AD.
Indexed as
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What Socratic 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 Socratic graph.