A subset of NSAIDs lower amyloidogenic Aβ42 independently of cyclooxygenase activity

By S. Weggen, J. Eriksen, Pritam Das, S. Sagi, Rong Wang, C. Pietrzik, K. Findlay, Tawnya E. Smith, M. Murphy, T. Bulter and 4 more. Nature, 2001

1,434 citations recorded by the source corpus.

Subfields: Oncology, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/d008869746f3afd7504d2ec0ac4d409037c7e229

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Oncology

1. D. Holtzman

In Pharmacology

1. D. Holtzman
2. F. LaFerla
3. G. Wenk
4. J. Long
5. S. Oddo
6. T. Wyss‐Coray
7. D. Selkoe
8. M. Kitazawa

In Physiology

1. Michael T. Heneka
2. D. Holtzman
3. J. Long
4. D. Selkoe
5. F. LaFerla
6. Martin Citron
7. John Hardy
8. M. O’Banion

Citations in the corpus

• Inflammation in Alzheimer disease: driving force, bystander or beneficial response? (2006, background): “Numerous in vitro studies have also shown that certain NSAIDs can modulate γ-secretase and the production of A&beta”
• Rho kinase, a promising drug target for neurological disorders (2005, background): “and an explanation for these data was provided with the observation that a subset of NSAIDs (ibuprofen, sulindac sulphide and indomethacin) reduced Aβ42 levels, independent of their effects on cyclooxygenase (COX) activit”
• Inflammatory processes in Alzheimer's disease. (2007, positive): “It has been shown that astrocytes throughout the entorhinal cortex of AD patients gradually accumulate Aβ1–42 positive material, and the amount of this material correlates positively with the extent of local AD pathology.”
• Protein aggregation diseases: pathogenicity and therapeutic perspectives (2010, background): “Drugs that modulate γ-secretase activity in this manner include non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofe”
• Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019, positive): “The first GSMs were discovered by recognizing that ibuprofen, indomethacin and sulindac reduce Abeta42 levels (Weggen et al., 2001) through modulation of gammasecretase activity (Eriksen et al.”
• APP mouse models for Alzheimer's disease preclinical studies (2017, neutral): “Further work into the potential of tackling c -secretase in a safe manner is based on overexpressing mice (Weggen et al , 2001) and novel insights into more safe approaches continue (De Strooper, 2014), illustrating the utility of the overexpression paradigm for certain types of preclinical studies…”
• A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines (2012, background): “ibuprofen, indomethacin, and sulindac sulphide were shown to decrease the Aβ-42 peptide by up to 80% in cultured cells (effect not observed with naproxen, celecoxib, or aspirin) [183].”