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Tau pathology in cognitively normal older adults
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Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer's disease
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Presence of tau pathology within foetal neural allografts in patients with Huntington's and Parkinson's disease
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Cerebrospinal fluid total tau concentration predicts clinical phenotype in Huntington's disease
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Caspase-2 cleavage of tau reversibly impairs memory
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Selected CSF biomarkers indicate no evidence of early neuroinflammation in Huntington disease
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Decreased glycogen synthase kinase-3 levels and activity contribute to Huntington's disease
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Mutant huntingtin alters Tau phosphorylation and subcellular distribution
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Localized changes to glycogen synthase kinase-3 and collapsin response mediator protein-2 in the Huntington's disease affected brain
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Huntington's disease is a four-repeat tauopathy with tau nuclear rods
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Mice lacking caspase-2 are protected from behavioral changes, but not pathology, in the YAC128 model of Huntington disease
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Tau oligomers impair memory and induce synaptic and mitochondrial dysfunction in wild-type mice
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Combined Treatment with the Mood Stabilizers Lithium and Valproate Produces Multiple Beneficial Effects in Transgenic Mouse Models of Huntington's Disease
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Genetic and pharmacological inhibition of calcineurin corrects the BDNF transport defect in Huntington's disease
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HUMAN MOLECULAR GENETICS (2006)
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Tau exons 2 and 10, which are misregulated in neurodegenerative diseases, are partly regulated by silencers which bind a SRp30c•SRp55 complex that either recruits or antagonizes htra2β1
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Microtubule destabilization and nuclear entry are sequential steps leading to toxicity in Huntington's disease
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Neuropathogenic forms of huntingtin and androgen receptor inhibit fast axonal transport
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Chronic lithium chloride treatment has variable effects on motor behaviour and survival of mice transgenic for the Huntington's disease mutation
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The IGF-1/Akt pathway is neuroprotective in Huntington's disease and involves huntingtin phosphorylation by Akt
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