G. Bu
Physiology · 2007–2019
A researcher in the Science corpus: 7 papers; trusts 13 researchers and is trusted by 12 researchers here, as inferred from the citation graph.
Subfields
- Physiology — 126 citations into it; #224 of 2,276 by trust here, #656 by citations
- Neurology — 51 citations into it
- Molecular Biology — 47 citations into it
- Cellular and Molecular Neuroscience — 39 citations into it
- Pharmacology — 19 citations into it; #121 of 1,112 by trust here, #287 by citations
- Cell Biology — 13 citations into it
- Genetics — 13 citations into it
- Oncology — 13 citations into it
Whom G. Bu trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
- D. Selkoe
- Lars Bertram
- G. Thinakaran
- D. Holtzman
- Rudolph E. Tanzi
- R. Deane
- Xi He
- J. Palop
- Jungsu Kim
- Christian Haass
Who trusts G. Bu overall
- D. Holtzman
- Martin Citron
- J. Herz
- Yangling Mu
- Nibaldo C. Inestrosa
- Yadong Huang
- Weifeng Zhang
- Fred H. Gage
Papers from G. Bu's perspective
Ordered by how strongly the researchers G. Bu trusts endorse each paper. Same corpus, a different order for every researcher.
- Transport Pathways for Clearance of Human Alzheimer's Amyloid β-Peptide and Apolipoproteins E and J in the Mouse Central Nervous System (Journal of Cerebral Blood Flow and Metabolism)
- Regulation of NMDA receptor trafficking by amyloid-β (Nature Neuroscience)
- Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease. (Neuron)
- Intraneuronal Aβ Causes the Onset of Early Alzheimer’s Disease-Related Cognitive Deficits in Transgenic Mice
- Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways (Nature Neuroscience)
- Apolipoprotein E isoform-dependent amyloid deposition and neuritic degeneration in a mouse model of Alzheimer's disease. (Proceedings of the National Academy of Sciences of the United States of America)
- The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease (Nature Genetics)
- Clearance of Alzheimer's amyloid-ss(1-40) peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier. (Journal of Clinical Investigation)
- Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo (Nature)
- ApoE promotes the proteolytic degradation of Abeta. (Neuron)
Their papers
- Apolipoprotein E and Alzheimer disease: risk, mechanisms, and therapy (2013) — 3,248 citations
- Apolipoprotein E and Alzheimer disease: pathobiology and targeting strategies (2019) — 1,192 citations
- TREM2 is a receptor for β-amyloid which mediates microglial function (2018) — 642 citations
- Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease. (2012) — 774 citations
- Apolipoprotein E and its receptors in Alzheimer's disease: pathways, pathogenesis and therapy (2009) — 1,108 citations
- Endocytosis is required for synaptic activity-dependent release of amyloid-beta in vivo. (2008) — 660 citations
- The γ/σ1 and α/σ2 Hemicomplexes of Clathrin Adaptors AP-1 and AP-2 Harbor the Dileucine Recognition Site (2007) — 160 citations