T. Spires-Jones
Physiology · 2008–2014
A researcher in the Science corpus: 4 papers; trusts 1 researcher and is trusted by 0 researchers here, as inferred from the citation graph.
Subfields
- Physiology — 64 citations into it
Whom T. Spires-Jones trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
Papers from T. Spires-Jones's perspective
Ordered by how strongly the researchers T. Spires-Jones trusts endorse each paper. Same corpus, a different order for every researcher.
- Regulation of NMDA receptor trafficking by amyloid-β (Nature Neuroscience)
- Oligomeric amyloid β associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques (Proceedings of the National Academy of Sciences of the United States of America)
- Tau-mediated neurodegeneration in Alzheimer's disease and related disorders (Nature Reviews Neuroscience)
- Propagation of Tau Misfolding from the Outside to the Inside of a Cell* (Journal of Biological Chemistry)
- Dendritic spines of CA 1 pyramidal cells in the rat hippocampus: serial electron microscopy with reference to their biophysical characteristics
- The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics (Science)
- Exogenous Induction of Cerebral ß-Amyloidogenesis Is Governed by Agent and Host (Science)
- β-Amyloid Stimulation of Microglia and Monocytes Results in TNFα-Dependent Expression of Inducible Nitric Oxide Synthase and Neuronal Apoptosis (Journal of Neuroscience)
- Bone marrow-derived microglia play a critical role in restricting senile plaque formation in Alzheimer's disease. (Neuron)
- Alzheimer's Disease Is a Synaptic Failure (Science)
Their papers
- Rapid appearance and local toxicity of amyloid-β plaques in a mouse model of Alzheimer’s disease (2008) — 889 citations
- The intersection of amyloid beta and tau at synapses in Alzheimer’s disease (2014) — 1,070 citations
- Propagation of tau pathology in a model of early Alzheimer’s disease (2012) — 1,415 citations
- Oligomeric amyloid β associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques (2009) — 857 citations