The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics
By John Hardy, D. Selkoe. Science, 2002
2,965 citations recorded by the source corpus.
Subfields: Molecular Biology, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/9cfbc163abbc8be0348ad13f9e31045f3704e019
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- D. Holtzman
- John C. Morris
- John Hardy
- A. Serrano‐Pozo
- John S. K. Kauwe
- Harald Hampel
- Rudolph E. Tanzi
- Martin Dichgans
In Pharmacology
- Rudolph E. Tanzi
- Harald Hampel
- M. Kitazawa
- Bradley T. Hyman
- George Bartzokis
- A. Caccamo
- Sangram S. Sisodia
- D. Holtzman
In Physiology
- D. Holtzman
- John Hardy
- John C. Morris
- Bradley T. Hyman
- R. Ransohoff
- Rudolph E. Tanzi
- Nick C Fox
- F. LaFerla
Citations in the corpus
- Heterogeneity of CNS myeloid cells and their roles in neurodegeneration (2011, background): “The essential neuropathological character of Alzheimer's disease entails the aggregation and accumulation of intracellular and extracellular component”
- Amyloid deposition precedes tangle formation in a triple transgenic model of Alzheimer's disease. (2003, background): “Astrogliosis is a prominent feature of AD neuropathology [1,3].”
- Calcium dyshomeostasis and intracellular signalling in alzheimer's disease (2002, background): “Its primacy has been manifested in the 'amyloid-cascade hypothesis', which posits that the accumulation of Aβ (resulting from overproduction, altered processing or a failure of clearance mechanisms) is the initiating molecular event that triggers neurodegeneration in sporadic and familial Alzheimer'”