ReviewJournal of molecular neuroscience : MN2002
Cdk5 as a drug target for the treatment of Alzheimer's disease.
Review in Journal of molecular neuroscience : MN, 2002. 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, 70 citations in OpenAlex.
- LIDDIA: Language-based Intelligent Drug Discovery Agent.Proceedings of the Conference on Empirical Methods in Natural Language Processing. Conference on Empirical Methods in Natural Language Processing · 2025Article
- Targeting a Tau Kinase Cdk5, Cyclin-Dependent Kinase: A Blood-Based Diagnostic Marker and Therapeutic Earmark for Alzheimer's Disease.Biomolecules · 2025Article
- Natural products against tau hyperphosphorylation-induced aggregates: Potential therapies for Alzheimer's disease.Archiv der Pharmazie · 2025Review
- Genetic knockdown of DYRK1A attenuates cognitive impairment, Aβ pathology, tauopathy and neuroinflammatory responses in mouse models of AD.Frontiers in immunology · 2025Article
- Oxidative stress: from molecular studies to clinical intervention strategies.Frontiers in molecular biosciences · 2025Review
- Synthesis of novel hybrids of 1,2,3-triazoles-hydrazone: targeting cholinesterases and Alzheimer's related genes.Future medicinal chemistry · 2024Article
- APPsα rescues CDK5 and GSK3β dysregulation and restores normal spine density in Tau transgenic mice.Frontiers in cellular neuroscience · 2023Article
- Semaphorins in Adult Nervous System Plasticity and Disease.Frontiers in synaptic neuroscience · 2021Review
- Review
- Characterization of the CDK5 gene in Apis cerana cerana (AccCDK5) and a preliminary identification of its activator gene, AccCDK5r1.Cell stress & chaperones · 2018Article
- TFP5 peptide, derived from CDK5-activating cofactor p35, provides neuroprotection in early-stage of adult ischemic stroke.Scientific reports · 2017Article
- Curcumin Ameliorates Neuroinflammation, Neurodegeneration, and Memory Deficits in p25 Transgenic Mouse Model that Bears Hallmarks of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2017Article
- TFP5, a Peptide Inhibitor of Aberrant and Hyperactive Cdk5/p25, Attenuates Pathological Phenotypes and Restores Synaptic Function in CK-p25Tg Mice.Journal of Alzheimer's disease : JAD · 2017Article
- The interaction of Munc 18 (p67) with the p10 domain of p35 protects in vivo Cdk5/p35 activity from inhibition by TFP5, a peptide derived from p35.Molecular biology of the cell · 2016Article
- Behind the curtain of tauopathy: a show of multiple players orchestrating tau toxicity.Cellular and molecular life sciences : CMLS · 2016Review
- Tolfenamic acid reduces tau and CDK5 levels: implications for dementia and tauopathies.Journal of neurochemistry · 2015Article
- Consensus models for CDK5 inhibitors in silico and their application to inhibitor discovery.Molecular diversity · 2015Article
- Specific inhibition of p25/Cdk5 activity by the Cdk5 inhibitory peptide reduces neurodegeneration in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- A truncated peptide from p35, a Cdk5 activator, prevents Alzheimer's disease phenotypes in model mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- The role of CDK5 and GSK3B kinases in hyperphosphorylation of microtubule associated protein tau (MAPT) in Alzheimer's disease.Bioinformation · 2013Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclin-dependent kinase-5 (cdk5) is suggested to play a role in tau phosphorylation and contribute to the pathogenesis of Alzheimer's disease (AD). One of its activators, p25, is dramatically increased in AD brains where p25 and cdk5 are colocalized with neurofibrillary tangles. Several animal models have shown a correlation of p25/cdk5 activities with tau phosphorylation. Overexpression of p25/cdk5 in nueronal cultures not only leads to tau phosphorylation but also cytoskeletal abnormalities and neurodegeneration. Therefore, cdk5 kinase inhibitors are potential therapeutic agents for the treatment of AD. Availability of potent, selective, brain permeable cdk5 inhibitors and relevant animal models in which their efficacy can be treated will be critical in the development of these inhibitors.
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.