Role of tau protein in both physiological and pathological conditions.

By J. Ávila, J. Lucas, Mar Pérez, F. Hernández. Physiological Reviews, 2004

972 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/4b90c4945d8854bd1beb5c9ce986d3e206b4d93a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. D. Rubinsztein
2. Fiona M Menzies
3. Cahir O'Kane
4. J. Isaac
5. K. Ashe
6. Y. Wang
7. G. Collingridge
8. B. Lamb

In Pharmacology

1. D. Rubinsztein

In Physiology

1. K. Ashe
2. D. Rubinsztein
3. D. Selkoe

Citations in the corpus

• LTP inhibits LTD in the hippocampus via regulation of GSK3beta. (2007, positive): “Of particular relevance to neurological disorders, GSK3β has been shown to bind to and phosphorylate both presenilin-1 and tau; proteins implicated in the aetiology of Alzheimer’s disease (Avila et al., 2004; Hanger et al., 1992; Kirschenbaum et al., 2001).”
• Characteristics of two distinct clinical phenotypes in pathologically proven progressive supranuclear palsy: Richardson's syndrome and PSP-parkinsonism. (2005, background): “The factors surrounding the pathogenicity of tau are still to be fully elucidated, although the degree to which tau accumulation is the primary event probably varies in different disease processes (Avila et al., 2004; Forman, 2004; Schraen-Maschke et al., 2004).”
• Inflammation as a central mechanism in Alzheimer's disease (2018, background): “remove tau from microtubules, allowing transport, followed by dephosphorylation to return tau to the microtubule [28].”
• Rapamycin alleviates toxicity of different aggregate-prone proteins. (2006, background): “Rapamycin decreased toxicity in flies expressing both wild-type tau and mutant tau that causes familial fronto-temporal dementia (40,41).”
• Tau mislocalization to dendritic spines mediates synaptic dysfunction independently of neurodegeneration (2010, methodology): “These hypotheses may explain how tau induces neurodegeneration, which correlates well with symptoms (re- viewed in Buée et al., 2000; Avila et al., 2004; Brandt et al., 2005) but do not address how tau diminishes brain function at the preclinical stages of disease immediately preceding…”