The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
APOE 4 polymorphism results in early cognitive deficits in an EAE model
Abstract
Recent clinical studies have identified an association between APOE 4 and cognitive deficits in patients with multiple sclerosis. We induced experimental autoimmune encephalomyelitis (EAE) in APOE knockout (KO) and human APOE 4 knockin (E4) mice to study the interaction of APOE and neuroinflammation on cognition. After EAE induction, KO and E4 showed significant deficits in spatial learning and recall. Regional decreases in choline acetyltransferase localized to the hippocampus. Induction of EAE in a transgenic APOE animal provides a template from which we can decipher the role APOE has on cognition in the context of neuroinflammation.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Recently, several studies have shown that APOE4 is associated with increased innate immune reactivity and enhanced cytokine secretion in primary microglia and peripheral macrophages in various animal models as well as human subjects [31–42].”
From 25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner (2020) · cites this paper as [37]
Citations
Cites
Cognitive dysfunction in multiple sclerosis.: II. Impact on employment and social functioning
Rao, S. M., Leo, G. J., Ellington, L., Nauertz, T., Bernardin, L., & Unverzagt, F. (1991) · Neurology · doi:10.1212/wnl.41.5.692 · Cited by 890
Apolipoprotein E structure: insights into function
Hatters, D. M., Peters-Libeu, C. A., & Weisgraber, K. H. (2006) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2006.06.008 · Cited by 583
Xu, P.-T., Schmechel, D., Rothrock-Christian, T., Burkhart, D. S., Qiu, H.-L., Popko, B., Sullivan, P., Maeda, N., Saunders, A. M., Roses, A. D., et al. (1996) · Neurobiology of Disease · doi:10.1006/nbdi.1996.0023 · Cited by 178
Hartman, R. E., Wozniak, D. F., Nardi, A., Olney, J. W., Sartorius, L., & Holtzman, D. M. (2001) · Experimental Neurology · doi:10.1006/exnr.2001.7715 · Cited by 157
Research works printed but not linked: 18
- Rao, 1991, Cognitive dysfunction in multiple sclerosis. I. Frequency, patterns, and prediction, Neurology, 41, 685, 10.1212/WNL.41.5.685 · DOI
- Shi, 2008, APOE epsilon 4 allele is associated with cognitive impairment in patients with multiple sclerosis, Neurology, 70, 185, 10.1212/01.wnl.0000264004.62612.44 · DOI
- Koutsis, 2007, APOE epsilon4 is associated with impaired verbal learning in patients with MS, Neurology, 68, 546, 10.1212/01.wnl.0000254468.51973.44 · DOI
- Knouff, 1999, Apo E structure determines VLDL clearance and atherosclerosis risk in mice, J. Clin. Invest., 103, 1579, 10.1172/JCI6172 · DOI · Paper page
- Zhao, 2008, A new EAE model of brain demyelination induced by intracerebroventricular pertussis toxin, Biochem. Biophys. Res. Commun., 370, 16, 10.1016/j.bbrc.2008.02.161 · DOI
- Tonra, 2002, Cerebellar susceptibility to experimental autoimmune encephalomyelitis in SJL/J mice: potential interaction of immunology with vascular anatomy, Cerebellum, 1, 57, 10.1080/147342202753203096 · DOI
- Morris, 1986, Selective impairment of learning and blockade of long-term potentiation by an N-methyl-d-aspartate receptor antagonist, AP5, Nature, 319, 774, 10.1038/319774a0 · DOI · Paper page
- Dotigny, 2008, Neuromodulatory role of acetylcholine in visually-induced cortical activation: behavioral and neuroanatomical correlates, Neuroscience, 154, 1607, 10.1016/j.neuroscience.2008.04.030 · DOI
- Pires, 2005, Cholinergic parameters and the retrieval of learned and re-learned spatial information: a study using a model of Wernicke–Korsakoff Syndrome, Behav. Brain Res., 162, 11, 10.1016/j.bbr.2005.02.032 · DOI
- Shi, 1999, Serum amyloid P is not present in amyloid beta deposits of a transgenic animal model, Neuroreport, 10, 3229, 10.1097/00001756-199910190-00019 · DOI
- Sternberger, 1986, The unlabeled antibody method: comparison of peroxidase–antiperoxidase with avidin–biotin complex by a new method of quantification, J. Histochem. Cytochem., 34, 599, 10.1177/34.5.3517144 · DOI
- Anderson, 1998, Behavioural, physiological and morphological analysis of a line of apolipoprotein E knockout mouse, Neuroscience, 85, 93, 10.1016/S0306-4522(97)00598-8 · DOI · Paper page
- Mahley, 2006, Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer’s disease, Proc. Natl. Acad. Sci. USA, 103, 5644, 10.1073/pnas.0600549103 · DOI · Paper page
- Weisgraber, 1996, Human apolipoprotein E: the Alzheimer’s disease connection, FASEB J., 10, 1485, 10.1096/fasebj.10.13.8940294 · DOI
- Pham, 2005, The receptor binding domain of apolipoprotein E is responsible for its antioxidant activity, Biochemistry, 44, 7577, 10.1021/bi0472696 · DOI
- Hoe, 2005, Multiple pathways of apolipoprotein E signaling in primary neurons, J. Neurochem., 93, 145, 10.1111/j.1471-4159.2004.03007.x · DOI · Paper page
- Saito, 2004, Contributions of domain structure and lipid interaction to the functionality of exchangeable human apolipoproteins, Prog. Lipid Res., 43, 350, 10.1016/j.plipres.2004.05.002 · DOI
- D’Intino, 2005, Cognitive deficit associated with cholinergic and nerve growth factor down-regulation in experimental allergic encephalomyelitis in rats, Proc. Natl. Acad. Sci. USA, 102, 3070, 10.1073/pnas.0500073102 · DOI
Cited by
Sorted by citations
25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner
Wong, M. Y., Lewis, M., Doherty, J. J., Shi, Y., Cashikar, A. G., Amelianchik, A., Tymchuk, S., Sullivan, P. M., Qian, M., Covey, D. F., et al. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01869-3 · Cited by 121
Apolipoprotein E Genotype Affects Size of ApoE Complexes in Cerebrospinal Fluid
Heinsinger, N. M., Gachechiladze, M. A., & Rebeck, G. W. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw067 · Cited by 74
Metadata
- Authors
- Tu, J.-L., Zhao, C.-B., Vollmer, T., Coons, S., Lin, H.-J., Marsh, S., Treiman, D. M., & Shi, J.
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2009-07
- Volume
- 384
- Issue
- 4
- Pages
- 466-470
- ISSN
- 0006-291X
- Cited by
- 29
- References
- 4
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: APOE 4 polymorphism results in early cognitive deficits in an EAE model. https://app.cochat.ai/papers/10.1016/j.bbrc.2009.04.153
- The paper
- Tu, J.-L., Zhao, C.-B., Vollmer, T., Coons, S., Lin, H.-J., Marsh, S., Treiman, D. M., & Shi, J. (2009). APOE 4 polymorphism results in early cognitive deficits in an EAE model. Biochemical and Biophysical Research Communications. https://doi.org/10.1016/j.bbrc.2009.04.153
