Synapse loss and microglial activation precede tangles in a P301S tauopathy mouse model.

By Y. Yoshiyama, M. Higuchi, Bin Zhang, Shu-ming Huang, N. Iwata, T. Saido, J. Maeda, T. Suhara, John Q. Trojanowski, V. Lee. Neuron, 2007

2,085 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/2b3b111d9075e121e4c1a4974ed7c73f77101f61

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. V. Lee
2. Annabelle C. Singer
3. John Q. Trojanowski
4. E. Masliah
5. Emery N. Brown
6. K. Ashe
7. Robin J. M. Franklin
8. Ed Boyden

In Neurology

1. V. Lee
2. Jing L Guo
3. John Q. Trojanowski
4. E. Masliah
5. Bin Zhang
6. Annabelle C. Singer
7. Robin J. M. Franklin
8. Ed Boyden

In Physiology

1. V. Lee
2. Jing L Guo
3. John Q. Trojanowski
4. L. Mucke
5. Bin Zhang
6. E. Masliah
7. A. Serrano‐Pozo
8. K. Ashe

Citations in the corpus

• The acetylation of tau inhibits its function and promotes pathological tau aggregation (2011, methodology): “Using anti-ac-K280, we probed tau acetylation in mouse brain by immunohistochemistry (IHC) using two tau Tg mouse models that recapitulate tau pathology and NFT formation: PS19 monogenic mice expressing P301S mutant ta”
• Microglia in Neurological Diseases: A Road Map to Brain-Disease Dependent-Inflammatory Response (2018, background): “In the last years, several studies have shown that alterations in protein aggregation and neuroinflammation may begin at early stages of FTLD or AD (Yoshiyama et al., 2007; Heneka et al., 2014; Morales et al., 2014).”
• Synthetic Tau Fibrils Mediate Transmission of Neurofibrillary Tangles in a Transgenic Mouse Model of Alzheimer’s-like Tauopathy (2013, methodology): “Although aged PS19 mice develop tau pathology in the LC, it occurred only when animals show widespread tau aggregates, neuron loss, and motoric phenotypes (Yoshiyama et al., 2007; our unpublished data).”
• Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023, background): “Importantly, immunosuppression with FK506 significantly decreased tau pathology and increased lifespan in young P301S Tg mice, thereby demonstrating that microglial activation and neuroinflammation promoted the early progression of tauopathies.(395) The further study discovered that Cx3cl1 expressed”
• Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases (2015, background): “microglial activation and delay the tau-related neuropathology in P301S tau mice [122].”
• Distinct tau prion strains propagate in cells and mice and define different tauopathies (2014, positive): “Transgenic mice expressing FL human tau 4R1N P301S under the murine prion promoter (Yoshiyama et al., 2007) were maintained on a B6C3 background.”
• Multi-sensory gamma stimulation ameliorates Alzheimer’s-associated pathology and improves cognition. (2019, background): “…Reduces Tau Phosphorylation and Seeding in AC and Hippocampus Tau phosphorylation at specific amino acid residues is a classical AD hallmark, and we previously showed that visual GENUS reduced tau hyperphosphorylation in another AD-associated mouse model, Tau P301S mice (Yoshiyama et al., 2007).”
• Mechanisms of tau-induced neurodegeneration (2009, neutral): “In P301S tau transgenic mice, a selective decrease in mitochondria and RER has been observed [214].”
• A role for motoneuron subtype–selective ER stress in disease manifestations of FALS mice (2009, background): “Interestingly, early losses in synaptic vesicles and synapses have been reported in several neurodegenerative disease”