ReviewNeuromolecular medicine2002
Fast axonal transport misregulation and Alzheimer's disease.
Review in Neuromolecular medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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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
46 citing papers in PubMed, 93 citations in OpenAlex.
- Review
- Krabbe disease: New hope for an old disease.Neuroscience letters · 2021Review
- Age-Dependent Decline in Synaptic Mitochondrial Function Is Exacerbated in Vulnerable Brain Regions of Female 3xTg-AD Mice.International journal of molecular sciences · 2020Article
- Administration of the benzodiazepine midazolam increases tau phosphorylation in the mouse brain.Neurobiology of aging · 2019Article
- Advances in the Potential Biomarkers of Epilepsy.Frontiers in neurology · 2019Review
- The Role of Axon Transport in Neuroprotection and Regeneration.Developmental neurobiology · 2018Review
- Differential effect of amyloid beta peptides on mitochondrial axonal trafficking depends on their state of aggregation and binding to the plasma membrane.Neurobiology of disease · 2018Article
- Axonal Degeneration in Tauopathies: Disease Relevance and Underlying Mechanisms.Frontiers in neuroscience · 2017Review
- Prion protein inhibits fast axonal transport through a mechanism involving casein kinase 2.PloS one · 2017Article
- HIV Glycoprotein Gp120 Impairs Fast Axonal Transport by Activating Tak1 Signaling Pathways.ASN neuro · 2016Article
- Pseudophosphorylation of tau at S422 enhances SDS-stable dimer formation and impairs both anterograde and retrograde fast axonal transport.Experimental neurology · 2016Article
- Load-induced enhancement of Dynein force production by LIS1-NudE in vivo and in vitro.Nature communications · 2016Article
- Autophagic and lysosomal defects in human tauopathies: analysis of post-mortem brain from patients with familial Alzheimer disease, corticobasal degeneration and progressive supranuclear palsy.Acta neuropathologica communications · 2016Article
- Long-distance endosome trafficking drives fungal effector production during plant infection.Nature communications · 2014Article
- Notch signalling in adult neurons: a potential target for microtubule stabilization.Therapeutic advances in neurological disorders · 2013Article
- REGION-SPECIFIC NEURON AND SYNAPSE LOSS IN THE HIPPOCAMPUS OF APPTranslational neuroscience · 2013Article
- Axonal transport and neurodegenerative disease: can we see the elephant?Progress in neurobiology · 2012Review
- Cargo distributions differentiate pathological axonal transport impairments.Journal of theoretical biology · 2012Article
- Axonal transport of APP and the spatial regulation of APP cleavage and function in neuronal cells.Experimental brain research · 2012Review
- Phosphorylation in the amino terminus of tau prevents inhibition of anterograde axonal transport.Neurobiology of aging · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Pathological alterations in the microtubule-associated protein (MAP) tau are well-established in a number of neurodegenerative disorders, including Alzheimer's Disease (AD), frontotemporal dementia (FTD), progressive supranuclear palsy (PSP), and others. Tau protein and in some cases, neurofilament subunits exhibit abnormal phosphorylation on specific serine and threonine residues in these diseases. A large body of biochemical, genetic, and cell biological evidence implicate two major serine-threonine protein kinases, glycogen synthase kinase 3 (GSK-3) and cyclin-dependent kinase 5 (CDK5) as major kinases responsible for both normal and pathological phosphorylation of tau protein in vivo. What remains unclear is whether tau phosphorylation and/or neurofibrillary tangle (NFT) formation are causal or secondary to initiation of neuronal pathology. In fact, many studies have indicated that tau misphosphorylation is not the causal event. Interestingly, some of these kinase and phosphatase activities have recently merged as key regulators of fast axonal transport (FAT). Specifically, CDK5 and GSK-3 have been recently shown to regulate kinesin-driven motility. Given the essential role of FAT in neuronal function, an alternate model for pathogenesis can be proposed. In this model, misregulation of FAT induced by an imbalance in specific kinase-phosphatase activities within neurons represents an early and critical step for the initiation of neuronal pathology. Such a model may explain many of the unique characteristics of late onset of neurological diseases such as AD.
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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.