M. Block

Neurology · Nature Reviews Neuroscience · 2004–2010

A researcher in the Science corpus: 7 papers; trusts 11 researchers and is trusted by 10 researchers here, as inferred from the citation graph.

Subfields

Whom M. Block trusts overall

Their strongest outbound trust, strongest first, inferred from their citations.

  1. H. Forman
  2. Jau-Shyong Hong
  3. S. Lehnardt
  4. G. Wenk
  5. A. Nimmerjahn
  6. Bin Liu
  7. Wolfgang Streit

Who trusts M. Block overall

  1. Melinda E Lull
  2. M. Tansey
  3. P. Whitton
  4. Wei-Wei Chen
  5. David J. Loane
  6. Yuanyuan Tang
  7. S. Lehnardt
  8. Rafael Franco
  9. U. Hanisch
  10. J. Felger

Papers from M. Block's perspective

Ordered by how strongly the researchers M. Block trusts endorse each paper. Same corpus, a different order for every researcher.

  1. Regional Difference in Susceptibility to Lipopolysaccharide-Induced Neurotoxicity in the Rat Brain: Role of Microglia (Journal of Neuroscience)
  2. NADPH Oxidase Mediates Lipopolysaccharide-induced Neurotoxicity and Proinflammatory Gene Expression in Activated Microglia* (Journal of Biological Chemistry)
  3. Innate immunity: the missing link in neuroprotection and neurodegeneration? (Nature Reviews Neuroscience)
  4. Bone marrow-derived microglia play a critical role in restricting senile plaque formation in Alzheimer's disease. (Neuron)
  5. Activation of innate immunity in the CNS triggers neurodegeneration through a Toll-like receptor 4-dependent pathway (Proceedings of the National Academy of Sciences of the United States of America)
  6. Aggregated α‐synuclein activates microglia: a process leading to disease progression in Parkinson's disease (The FASEB Journal)
  7. In-vivo measurement of activated microglia in dementia. (The Lancet)
  8. The Toll-Like Receptor TLR4 Is Necessary for Lipopolysaccharide-Induced Oligodendrocyte Injury in the CNS (Journal of Neuroscience)
  9. Ubiquitination of a New Form of α-Synuclein by Parkin from Human Brain: Implications for Parkinson's Disease (Science)
  10. Altered proteasomal function in sporadic Parkinson's disease. (Experimental Neurology)

Their papers