CommentaryPHF and PHF-like fibrils –cause or consequence?
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Synthesis of (R,S)-isoproterenol, an inhibitor of tau aggregation, as an <sup>11</sup>C-labeled PET tracer via reductive alkylation of (R,S)-norepinephrine with [2-<sup>11</sup>C]acetone
2019, Bioorganic and Medicinal Chemistry LettersEarly depletion of CA1 neurons and late neurodegeneration in a mouse tauopathy model
2017, Brain ResearchCitation Excerpt :Similar is assumed for human brains where neurons are believed to bear with their NFT material relatively well for years (Bobinski et al., 1998; Morsch et al., 1999). Consequently, tau aggregates are considered neither acutely toxic nor incompatible with long-term neuronal survival (Ihara, 2001). Neurodegeneration was observed at 48 W when 43% of CA1 neurons were lost in the rTg4510 mice.
The Many Faces of Tau
2011, NeuronCitation Excerpt :These include AD; frontotemporal lobar degeneration with tau inclusions (FTLD-tau) such as Pick's disease, progressive supranuclear palsy, and corticobasal degeneration; agyrophillic grain disease; some prion diseases; amyotrophic lateral sclerosis/parkinsonism-dementia complex; chronic traumatic encephalopathy; and some genetic forms of Parkinson's disease (Lee et al., 2001; Omalu et al., 2011; Rajput et al., 2006; Santpere and Ferrer, 2009). Although associations per se cannot prove cause-effect relationships, tau inclusions are widely thought to contribute to the pathogenesis of these disorders because they occur in specific brain regions whose functions are altered by these conditions, and NFT formation correlates with the duration and progression of AD (Giannakopoulos et al., 2003; Ihara, 2001). Tau inclusions also appear to modulate the clinical features of other neurodegenerative diseases.
Increased levels of granular tau oligomers: An early sign of brain aging and Alzheimer's disease
2006, Neuroscience ResearchTau phosphorylation in Alzheimer's disease: Pathogen or protector?
2005, Trends in Molecular MedicineTau modifiers as therapeutic targets for Alzheimer's disease
2005, Biochimica et Biophysica Acta - Molecular Basis of Disease