ArticleMolecular biology of the cell2013
Amyloid-β oligomers induce tau-independent disruption of BDNF axonal transport via calcineurin activation in cultured hippocampal neurons.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 67 citations in OpenAlex.
- Molecular architects of memory: BDNF/TrkB signaling and trafficking in neuronal plasticity and memory.Molecular psychiatry · 2026Review
- Peptide-based therapeutics in the management of Alzheimer's disease (AD) and their potential to develop novel strategies.Metabolic brain disease · 2026Review
- Somatostatin: Linking Cognition and Alzheimer Disease to Therapeutic Targeting.Pharmacological reviews · 2024Review
- Heterogeneity of factors associated with cognitive decline and cortical atrophy in early- versus late-onset Alzheimer's disease.Scientific reports · 2024Article
- Synaptic proteasome is inhibited in Alzheimer's disease models and associates with memory impairment in mice.Communications biology · 2023Article
- Article
- Connectome-based biophysics models of Alzheimer's disease diagnosis and prognosis.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Aß Pathology and Neuron-Glia Interactions: A Synaptocentric View.Neurochemical research · 2023Review
- Modulation of Mitochondrial Function as a Therapeutic Strategy for Neurodegenerative Diseases.The journal of prevention of Alzheimer's disease · 2023Review
- Maternal immune activation-induced proBDNF-mediated neural information processing dysfunction at hippocampal CA3-CA1 synapses associated with memory deficits in offspring.Frontiers in cell and developmental biology · 2022Article
- Mechanism by Which Aluminum Regulates the Abnormal Phosphorylation of the Tau Protein in Different Cell Lines.ACS omega · 2021Article
- Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021Review
- An Unbalanced Synaptic Transmission: Cause or Consequence of the Amyloid Oligomers Neurotoxicity?International journal of molecular sciences · 2021Review
- Targeting increased levels of APP in Down syndrome: Posiphen-mediated reductions in APP and its products reverse endosomal phenotypes in the Ts65Dn mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Article
- Effects of Alzheimer's and Vascular Pathologies on Structural Connectivity in Early- and Late-Onset Alzheimer's Disease.Frontiers in neuroscience · 2021Article
- Prevention of mitochondrial impairment by inhibition of protein phosphatase 1 activity in amyotrophic lateral sclerosis.Cell death & disease · 2020Article
- Tau is not necessary for amyloid-β-induced synaptic and memory impairments.The Journal of clinical investigation · 2020Article
- Cotinine and 6-Hydroxy-L-Nicotine Reverses Memory Deficits and Reduces Oxidative Stress in AβAntioxidants (Basel, Switzerland) · 2020Article
- The Regulation of microRNAs in Alzheimer's Disease.Frontiers in neurology · 2020Review
- Protein Misfolding, Signaling Abnormalities and Altered Fast Axonal Transport: Implications for Alzheimer and Prion Diseases.Frontiers in cellular neuroscience · 2019Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Disruption of fast axonal transport (FAT) is an early pathological event in Alzheimer's disease (AD). Soluble amyloid-β oligomers (AβOs), increasingly recognized as proximal neurotoxins in AD, impair organelle transport in cultured neurons and transgenic mouse models. AβOs also stimulate hyperphosphorylation of the axonal microtubule-associated protein, tau. However, the role of tau in FAT disruption is controversial. Here we show that AβOs reduce vesicular transport of brain-derived neurotrophic factor (BDNF) in hippocampal neurons from both wild-type and tau-knockout mice, indicating that tau is not required for transport disruption. FAT inhibition is not accompanied by microtubule destabilization or neuronal death. Significantly, inhibition of calcineurin (CaN), a calcium-dependent phosphatase implicated in AD pathogenesis, rescues BDNF transport. Moreover, inhibition of protein phosphatase 1 and glycogen synthase kinase 3β, downstream targets of CaN, prevents BDNF transport defects induced by AβOs. We further show that AβOs induce CaN activation through nonexcitotoxic calcium signaling. Results implicate CaN in FAT regulation and demonstrate that tau is not required for AβO-induced BDNF transport disruption.
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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.