Folic Acid Deficiency and Homocysteine Impair DNA Repair in Hippocampal Neurons and Sensitize Them to Amyloid Toxicity in Experimental Models of Alzheimer's Disease

By I. Kruman, T. Kumaravel, A. Lohani, W. A. Pedersen, R. Cutler, Y. Kruman, N. Haughey, Jaewon Lee, M. Evans, Mark P. Mattson. Journal of Neuroscience, 2002

658 citations recorded by the source corpus.

Subfields: Nutrition and Dietetics, Rheumatology

View Paper: https://www.semanticscholar.org/paper/19daa6a4641458378a6f0bf3ea8b72c8f8de33d6

How researchers see this paper

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

1. Mark P. Mattson
2. T. Shea
3. R. Kaufman
4. J. Malhotra
5. C. Hetz
6. Michael T. Heneka
7. Randy L. Buckner
8. D. Ron

Citations in the corpus

• Orchestrating the unfolded protein response in health and disease. (2002, background): “Hyperhomocysteinemia is also associated with increased amyloid production and increased amyloid-mediated neuronal death in animal models of Alzheimer disease (80).”
• Folate and homocysteine metabolism in neural plasticity and neurodegenerative disorders. (2003, background): “excitotoxicity [75,76] (Table 2). A particularly insidious aspect of the neurotoxicity of folate deprivation and increased homocysteine is that they interact synergistically with, and potentiate, several of these factors (Table 1). For example, homocysteine or folate deprivation can potentiate Ab ne”