ArticleMagnetic resonance insights2010
Increased Human Wildtype Tau Attenuates Axonal Transport Deficits Caused by Loss of APP in Mouse Models.
Article in Magnetic resonance insights, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Manganese-Enhanced Magnetic Resonance Imaging: Application in Central Nervous System Diseases.Frontiers in neurology · 2020Review
- In Vivo Evaluation of Neuronal Transport in Murine Models of Neurodegeneration Using Manganese-Enhanced MRI.Methods in molecular biology (Clifton, N.J.) · 2018Article
- Manganese Enhanced MRI for Use in Studying Neurodegenerative Diseases.Frontiers in neural circuits · 2018Review
- Manganese-Enhanced Magnetic Resonance Imaging: Overview and Central Nervous System Applications With a Focus on Neurodegeneration.Frontiers in aging neuroscience · 2018Review
- Preclinical Magnetic Resonance Imaging and Spectroscopy Studies of Memory, Aging, and Cognitive Decline.Frontiers in aging neuroscience · 2016Review
- Pharmocologic treatment with histone deacetylase 6 inhibitor (ACY-738) recovers Alzheimer's disease phenotype in amyloid precursor protein/presenilin 1 (APP/PS1) mice.Alzheimer's & dementia (New York, N. Y.) · 2015Article
- Age-related decline in white matter integrity in a mouse model of tauopathy: an in vivo diffusion tensor magnetic resonance imaging study.Neurobiology of aging · 2014Article
- In vivo axonal transport deficits in a mouse model of fronto-temporal dementia.NeuroImage. Clinical · 2014Article
- The airbag problem-a potential culprit for bench-to-bedside translational efforts: relevance for Alzheimer's disease.Acta neuropathologica communications · 2013Review
- Non-invasive, in vivo monitoring of neuronal transport impairment in a mouse model of tauopathy using MEMRI.NeuroImage · 2013Article
- Global axonal transport rates are unaltered in htau mice in vivo.Journal of Alzheimer's disease : JAD · 2013Article
- Axonal transport and neurodegenerative disease: can we see the elephant?Progress in neurobiology · 2012Review
- Impact of repeated topical-loaded manganese-enhanced MRI on the mouse visual system.Investigative ophthalmology & visual science · 2012Article
- Deficits in axonal transport in hippocampal-based circuitry and the visual pathway in APP knock-out animals witnessed by manganese enhanced MRI.NeuroImage · 2012Article
- From axonal transport to mitochondrial trafficking: What can we learn from Manganese-Enhanced MRI studies in mouse models of Alzheimers disease?Current medical imaging reviews · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Amyloid precursor protein (APP) is implicated in axonal elongation, synaptic plasticity, and axonal transport. However, the role of APP on axonal transport in conjunction with the microtubule associated protein tau continues to be debated. Here we measured in vivo axonal transport in APP knockout mice with Manganese Enhanced MRI (MEMRI) to determine whether APP is necessary for maintaining normal axonal transport. We also tested how overexpression and mutations of tau affect axonal transport in the presence or absence of APP. In vivo axonal transport reduced significantly in the absence of functional APP. Overexpression of human wildtype tau maintained normal axonal transport and resulted in a transient compensation of axonal transport deficits in the absence of APP. Mutant R406Wtau in combination with the absence of APP compounded axonal transport deficits and these deficits persisted with age. These results indicate that APP is necessary for axonal transport, and overexpression of human wildtype tau can compensate for the absence of APP at an early age.
Identifiers
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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.