Neurodegenerative tauopathies.
By V. Lee, M. Goedert, John Q. Trojanowski. Annual Review of Neuroscience, 2001
2,045 citations recorded by the source corpus.
Subfields: Neurology, Physiology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/8eb6355272daf41b8da72a5b18a4d8c67d8509cc
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Neurology
- V. Lee
- Dennis W. Dickson
- Brittany N. Dugger
- D. Selkoe
- M. Goedert
- Michael T. Heneka
- John Q. Trojanowski
- M. O’Banion
In Physiology
In Psychiatry and Mental health
- Michael T. Heneka
- M. O’Banion
- D. Selkoe
- Dennis W. Dickson
- Jessica R. Andrews-Hanna
- Brittany N. Dugger
- E. Masliah
- Randy L. Buckner
Citations in the corpus
- Alzheimer’s Disease and the β-Amyloid Peptide (2010, neutral): “The neurofibrillary tangles in the different diseases have some distinctive morphological features and may exhibit a distinct composition of tau isoforms that differs from AD [1].”
- Clinical Neurology and Epidemiology of the Major Neurodegenerative Diseases. (2018, background): “…with atrophy within the basal ganglia, subthalamus, and brainstem, and is characterized microscopically by dense fibrillary four-repeat tau (4R tauopathy) filaments, globose-appearing neurofibrillary tangles, and glial fibrillary tangles in astrocytes and oligodendrocytes (Lee et al. 2001).”
- GABAergic Interneuron Dysfunction Impairs Hippocampal Neurogenesis in Adult Apolipoprotein E4 Knock-in Mice (2009, background): “The major function of tau, which is abundant in the axons of neurons, is to bind and stabilize microtubules (Lee et al., 2001).”
- Abundant Tau Filaments and Nonapoptotic Neurodegeneration in Transgenic Mice Expressing Human P301S Tau Protein (2002, background): “In FTDP-17, the age of onset of disease varies, depending on the Tau mutation.”
- Inflammatory processes in Alzheimer's disease. (2007, positive): “AD brains show two characteristic lesions: extracellular deposits of β-amyloid peptides, so-called neuritic or senile plaques, and intracellular neurofibrillary tangles of hyperphosphorylated tau (Lee et al., 2001; Selkoe, 2003).”
- Molecular mechanisms of neurodegeneration in Alzheimer's disease. (2010, background): “This is accompanied by astrogliosis (9), microglial cell proliferation (10, 11) and the presence of neurofibrillary tangles composed of dystrophic neurites and hyperphosphorylated tau (5, 12-16).”
- Tau fragmentation, aggregation and clearance: the dual role of lysosomal processing. (2009, background): “Abnormal aggregates of Tau [neurofibrillary tangles, consisting of paired helical filaments (PHFs)] are hallmarks of several neurodegenerative diseases including Alzheimer disease (AD) and other tauopathies (1,2).”
- Role of tau protein in both physiological and pathological conditions. (2004, background): “Several good reviews dealing with specific features of tau have been published recently (32, 147, 160, 182, 254).”
- Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease (2018, background): “Tau pathologies are also seen in other neurodegenerative dementing disorders, such as frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), Pick’s disease (PiD), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), tangleonly ”