ArticleJournal of Alzheimer's disease : JAD2013
Global axonal transport rates are unaltered in htau mice in vivo.
Article in Journal of Alzheimer's disease : JAD, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Aberrant tau accumulation caused by MAPT mutations induces early pathological changes in axonal transport that are rescued by p38α inhibition.Nature neuroscience · 2026Article
- Pathological and physiological functional cross-talks of α-synuclein and tau in the central nervous system.Neural regeneration research · 2024Review
- A role for tau in learning, memory and synaptic plasticity.Scientific reports · 2018Article
- Differential Hyperphosphorylation of Tau-S199, -T231 and -S396 in Organotypic Brain Slices of Alzheimer Mice. A Model to Study Early Tau Hyperphosphorylation Using Okadaic Acid.Frontiers in aging neuroscience · 2018Article
- Human Tau Expression Does Not Induce Mouse Retina Neurodegeneration, Suggesting Differential Toxicity of Tau in Brain vs. Retinal Neurons.Frontiers in molecular neuroscience · 2018Article
- TDP-43 suppresses tau expression via promoting its mRNA instability.Nucleic acids research · 2017Article
- Tau Isoforms Imbalance Impairs the Axonal Transport of the Amyloid Precursor Protein in Human Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Intracellular amyloid β oligomers impair organelle transport and induce dendritic spine loss in primary neurons.Acta neuropathologica communications · 2015Article
- Axonal transport defects in Alzheimer's disease.Molecular neurobiology · 2015Review
- Motor and cognitive deficits in aged tau knockout mice in two background strains.Molecular neurodegeneration · 2014Article
- Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.The European journal of neuroscience · 2014Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Microtubule-based axonal transport is believed to become globally disrupted in Alzheimer's disease in part due to alterations of tau expression or phosphorylation. We previously showed that axonal transport rates along retinal ganglion axons are unaffected by deletion of normal mouse tau or by overexpression of wild-type human tau. Here, we report that htau mice expressing 3-fold higher levels of human tau in the absence of mouse tau also display normal fast and slow transport kinetics despite the presence of abnormally hyperphosphorylated tau in some neurons. In addition, markers of slow transport (neurofilament light subunit) and fast transport (snap25) exhibit normal distributions along optic axons of these mice. These studies demonstrate that human tau overexpression, even when associated with a limited degree of tau pathology, does not necessarily impair general axonal transport function in vivo.
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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.