Human Tau Aggregates Are Permissive to Protein Synthesis-Dependent Memory in Drosophila Tauopathy Models.

Tau-mediated axonal degeneration is prevented by activation of the WldS pathway.

Age-related changes in tau and autophagy in human brain in the absence of neurodegeneration.

Curcumin as a Holistic Treatment for Tau Pathology.

Suppression of tau-induced phenotypes by vitamin E demonstrates the dissociation of oxidative stress and phosphorylation in mechanisms of tau toxicity.

Conformational fingerprinting of tau variants and strains by Raman spectroscopy.

Conformational Evolution of Molecular Signatures during Amyloidogenic Protein Aggregation.

CSF1R inhibitor JNJ-40346527 attenuates microglial proliferation and neurodegeneration in P301S mice.

Insulin-Mediated Changes in Tau Hyperphosphorylation and Autophagy in a Drosophila Model of Tauopathy and Neuroblastoma Cells.

An evaluation of Drosophila as a model system for studying tauopathies such as Alzheimer's disease.

An assessment of the translational relevance of Drosophila in drug discovery.

Alzheimer's Disease and Type 2 Diabetes: A Critical Assessment of the Shared Pathological Traits.

Raman Spectroscopy: An Emerging Tool in Neurodegenerative Disease Research and Diagnosis.

Pyroglutamate and Isoaspartate modified Amyloid-Beta in ageing and Alzheimer's disease.

What is the evidence that tau pathology spreads through prion-like propagation?

Atypical, non-standard functions of the microtubule associated Tau protein.

EuroTau: towing scientists to tau without tautology.

Distinct phenotypes of three-repeat and four-repeat human tau in a transgenic model of tauopathy.

Corrigendum: Microtubule stabilising peptides rescue tau phenotypes in-vivo.

Microtubule stabilising peptides rescue tau phenotypes in-vivo.

Potential mechanisms and implications for the formation of tau oligomeric strains.

The use of human neurons for novel drug discovery in dementia research.

Rescue from tau-induced neuronal dysfunction produces insoluble tau oligomers.

Drosophila modelling axonal transport in the face of tau pathology.

Translation of Pre-Clinical Studies into Successful Clinical Trials for Alzheimer's Disease: What are the Roadblocks and How Can They Be Overcome?

Are tau aggregates toxic or protective in tauopathies?

NAP (davunetide) rescues neuronal dysfunction in a Drosophila model of tauopathy.

Low endogenous and chemical induced heat shock protein induction in a 0N3Rtau-expressing Drosophila larval model of Alzheimer's disease.

Drug repositioning for Alzheimer's disease.

What is the pathological significance of tau oligomers?

Twice is better: highlights of the second meeting focused on tau biology and pathology.

Increased throughput assays of locomotor dysfunction in Drosophila larvae.

Using Drosophila models of neurodegenerative diseases for drug discovery.

Modelling tauopathies in Drosophila: insights from the fruit fly.

Soluble hyper-phosphorylated tau causes microtubule breakdown and functionally compromises normal tau in vivo.

Insights from Drosophila models of Alzheimer's disease.

Two days of tau: a meeting focused on its biology and pathology.

Aβ exacerbates the neuronal dysfunction caused by human tau expression in a Drosophila model of Alzheimer's disease.

Disruption of neuronal function by soluble hyperphosphorylated tau in a Drosophila model of tauopathy.

Using Drosophila models to unravel pathogenic mechanisms that underlie neurodegeneration in tauopathies.

Modelling neurodegenerative diseases in Drosophila.

A comparison of the neuronal dysfunction caused by Drosophila tau and human tau in a Drosophila model of tauopathies.

Overexpression of tau results in defective synaptic transmission in Drosophila neuromuscular junctions.

Over-expression of tau results in defective synaptic transmission in Drosophila neuromuscular junctions.

GSK-3beta inhibition reverses axonal transport defects and behavioural phenotypes in Drosophila.

Alzheimer's disease-do tauists and baptists finally shake hands?

Dishevelled regulates the metabolism of amyloid precursor protein via protein kinase C/mitogen-activated protein kinase and c-Jun terminal kinase.