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Regulation of NMDA receptor trafficking by amyloid-β

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Microtubule-associated protein tau (tau) is a major antigenic component of paired helical filaments in Alzheimer disease.

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Tau Mislocalization to Dendritic Spines Mediates Synaptic Dysfunction Independently of Neurodegeneration

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S-Nitrosylation of Drp1 Mediates β-Amyloid-Related Mitochondrial Fission and Neuronal Injury

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Specific tau phosphorylation sites correlate with severity of neuronal cytopathology in Alzheimer's disease

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Trans-Synaptic Spread of Tau Pathology In Vivo

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Aβ Oligomers Induce Neuronal Oxidative Stress through an N-Methyl-D-aspartate Receptor-dependent Mechanism That Is Blocked by the Alzheimer Drug Memantine

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Soluble amyloid β-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration

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2010 Alzheimer's disease facts and figures

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Amyloid-β/Fyn–Induced Synaptic, Network, and Cognitive Impairments Depend on Tau Levels in Multiple Mouse Models of Alzheimer's Disease

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Physiological release of endogenous tau is stimulated by neuronal activity

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Metabotropic Glutamate Receptor 5 Is a Coreceptor for Alzheimer Aβ Oligomer Bound to Cellular Prion Protein

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Caspase activation precedes and leads to tangles

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Modulation of NMDA Receptor- Dependent Calcium Influx and Gene Expression Through EphB Receptors

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Tau Reduction Prevents Aβ-Induced Defects in Axonal Transport

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Synthetic amyloid-β oligomers impair long-term memory independently of cellular prion protein

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β-Amyloid Activates the Mitogen-Activated Protein Kinase Cascade via Hippocampal α7 Nicotinic Acetylcholine Receptors:<i>In Vitro</i>and<i>In Vivo</i>Mechanisms Related to Alzheimer's Disease

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Brain Insulin Resistance and Deficiency as Therapeutic Targets in Alzheimers Disease

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Memory Impairment in Transgenic Alzheimer Mice Requires Cellular Prion Protein

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Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficits

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Distinct Dendritic Spine and Nuclear Phases of Calcineurin Activation after Exposure to Amyloid-β Revealed by a Novel Fluorescence Resonance Energy Transfer Assay

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Insulin signalling promotes dendrite and synapse regeneration and restores circuit function after axonal injury

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Retinal ganglion cell dendrite pathology and synapse loss

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Dendritic and axonal mechanisms of Ca²⁺ elevation impair BDNF transport in Aβ oligomer–treated hippocampal neurons

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International courses Neuropathology

den Dunnen, W. F. A., & Wilfred, F. A. (2020)