Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer's disease.

By R. Mahley, K. Weisgraber, Yadong Huang. Proceedings of the National Academy of Sciences of the United States of America, 2006

947 citations recorded by the source corpus.

Subfields: Cell Biology, Cellular and Molecular Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/92ba28ef868a86ec18e7626607b34756f90758c1

How researchers see this paper

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

In Cell Biology

1. D. Selkoe
2. O. Maier
3. Roman Fischer
4. Juan Zhang
5. Qiang Liu
6. Martin Citron
7. G. Bu
8. Mark P. Mattson

In Cellular and Molecular Neuroscience

1. L. Mucke
2. J. Palop
3. G. Bu
4. D. Selkoe
5. Nga Bien-Ly
6. Y. Andrews-Zwilling
7. O. Maier
8. T. Bird

In Physiology

1. L. Mucke
2. J. Palop
3. G. Bu
4. D. Selkoe
5. Martin Citron
6. Mark P. Mattson
7. T. Bird
8. L. Bekris

Citations in the corpus

• The Role of Apolipoprotein E in Alzheimer’s Disease (2009, neutral): “One of the most extensively investigated direct toxic mechanisms involves the 29 kDa carboxyl-terminal-truncated fragment of apoE4 (amino acid 1–272 residues) (Mahley et al., 2007;Mahley et al., 2006).”
• Calcium and neurodegeneration (2007, background): “increased risk of AD compared to those with E2 or E3 isoforms (Mahley et al., 2006).”
• Interrelation of Oxidative Stress and Inflammation in Neurodegenerative Disease: Role of TNF (2015, background): “Furthermore, there is also evidence linking apoE4, the major risk factor to develop sporadic AD, with increased oxidative stress and mitochondrial dysfunction in hippocampal neurons [56].”
• Epilepsy and Cognitive Impairments in Alzheimer Disease (2009, background): “Although the mechanisms underlying this link remain to be fully elucidated, much evidence suggests that ApoE4 contributes to AD pathogenesis through both A -dependent and A -independent pathways.(19) Aberrant increases in network excitability may represent a critical convergence point for the advers”
• The role of microglia in amyloid clearance from the AD brain (2010, background): “Three common variants of ApoE (ApoE e2, e3 and e4) in humans differ in amino acids at positions 112 and 158 conferring differences in cholesterol efflux efficiency, lipidation status and receptor-binding affinity (Mahley et al. 2006a, b).”
• Amyloid-β Induced Neuronal Dysfunction in Alzheimer’s Disease: From Synapses toward Neural Networks (2010, background): “Among them, Aβ and the genetic risk factor apolipoprotein (apo)-E4 stand out on the basis of overwhelming genetic evidence and strong experimental dat”
• GABAergic Interneuron Dysfunction Impairs Hippocampal Neurogenesis in Adult Apolipoprotein E4 Knock-in Mice (2009, background): “However, the apoE isoforms differ in their ability to fulfill these functions (Huang, 2006a, 2006b; Huang et al., 2004; Mahley et al., 2006).”
• A network dysfunction perspective on neurodegenerative diseases (2006, neutral): “, genetic factors such as apolipoprotein-E isoform”
• Alzheimer's disease: strategies for disease modification (2010, background): “For example, by inhibiting a neuronal protease that — according to their model — generates a toxic APOE4 fragment or by developing 'structural correctors' — small molecules that would bind to APOE4 and block the intramolecular domain interaction that is characteristic of this isoform, thus convertin”
• Neurotoxicity of amyloid β-protein: synaptic and network dysfunction. (2012, background): “2008) or replacement of apoE4 function with apoE3-like function (Raber et al. 2000; Buttini et al. 2002; Mahley et al. 2006).”