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Mitochondrial oxidative stress contributes to the pathological aggregation and accumulation of tau oligomers in Alzheimer’s disease

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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

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Soluble pre-fibrillar tau and β-amyloid species emerge in early human Alzheimer’s disease and track disease progression and cognitive decline

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The diagnosis of dementia due to Alzheimer's disease: Recommendations from the National Institute on Aging‐Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease

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Extracellular low‐n oligomers of tau cause selective synaptotoxicity without affecting cell viability

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Neurodegenerative Tauopathies

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Granular Tau Oligomers as Intermediates of Tau Filaments

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Extracellular Tau Oligomers Produce An Immediate Impairment of LTP and Memory

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Characterization of Prefibrillar Tau Oligomers in Vitro and in Alzheimer Disease

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Tau blocks traffic of organelles, neurofilaments, and APP vesicles in neurons and enhances oxidative stress

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Tau Oligomer Pathology in Nucleus Basalis Neurons During the Progression of Alzheimer Disease

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Behavioral deficit, oxidative stress, and mitochondrial dysfunction precede tau pathology in P301S transgenic mice

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Amyloid Oligomers Exacerbate Tau Pathology in a Mouse Model of Tauopathy

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Oxidative stress mediates tau-induced neurodegeneration in Drosophila

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Tau oligomers impair memory and induce synaptic and mitochondrial dysfunction in wild-type mice

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Mitochondrial Oxidative Stress Causes Hyperphosphorylation of Tau

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Alterations in Glucose Metabolism Induce Hypothermia Leading to Tau Hyperphosphorylation through Differential Inhibition of Kinase and Phosphatase Activities: Implications for Alzheimer's Disease

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TOC1: Characterization of a Selective Oligomeric Tau Antibody

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Region-Specific Vulnerability to Oxidative Stress, Neuroinflammation, and Tau Hyperphosphorylation in Experimental Diabetes Mellitus Mice

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Increased Electron Paramagnetic Resonance Signal Correlates with Mitochondrial Dysfunction and Oxidative Stress in an Alzheimer’s disease Mouse Brain

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Antioxidants Rescue Mitochondrial Transport in Differentiated Alzheimer’s Disease Trans-Mitochondrial Cybrid Cells

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PINK1 Activation Attenuates Impaired Neuronal-Like Differentiation and Synaptogenesis and Mitochondrial Dysfunction in Alzheimer’s Disease Trans-Mitochondrial Cybrid Cells

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