Insulin and insulin-like growth factor expression and function deteriorate with progression of Alzheimer's disease: Link to brain reductions in acetylcholine
By E. Rivera, Alison H. Goldin, Noah Fulmer, Rosemarie Tavares, J. Wands, S. M. de la Monte. Journal of Alzheimer's Disease, 2005
719 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/d0f050b7116f3e8d4e14a9b3d60fc10c1c86b236
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Endocrinology, Diabetes and Metabolism
In Molecular Biology
In Physiology
- Julie A. Schneider
- David A. Bennett
- R. Wilson
- Zoe Arvanitakis
- John Q. Trojanowski
- C. Zhong
- Zhichun Chen
- C. Iadecola
Citations in the corpus
- Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, positive): “These alterations are involved in the progression of AD according to Braak staging (Rivera et al., 2005).”
- Trends in insulin resistance: insights into mechanisms and therapeutic strategy (2022, background): “For example, major abnormalities in AD brains include decreased mRNA and protein expression levels of insulin, insulin receptors, insulin receptor substrate 1 (IRS1) and IGF1/2, in addition to reduced protein indicators of downstream insulin signaling activity (including phosphorylated AKT (pAKT) an”
- Inflammation as a central mechanism in Alzheimer's disease (2018, background): “[255] Rivera EJ, Goldin A, Fulmer N, Tavares R, Wands JR, la Monte de SM.”
- Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. (2012, background): “A number of the findings at upstream levels of the pathway are consistent with insulin resistance as defined above, notably decreased basal activation of IRs (28); reduced insulin binding of the IR, even early in the disorder (27); increased serine phosphorylation (pS) of IRS-1 (29, 33, 37); and red”