The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Increased apolipoprotein E expression correlates with the onset of neuronal degeneration in the spinal cord of G93A-SOD1 mice
Abstract
Apolipoprotein E (apoE) genotype is well known as a risk factor for Alzheimer's disease, but more recently also has been associated with the incidence or disease progression of other neurological diseases including amyotrophic lateral sclerosis (ALS). In the present study we have examined the distribution of apoE in the spinal cord of transgenic mice with a familial ALS-linked superoxide dismutase 1 (G93A-SOD1) mutation. Western immunoblotting and immunocytochemistry showed a strong increase in apoE expression in G93A-SOD1 mice coincident with the onset of paralysis (age > 24 weeks). Increased apoE expression occurred in astrocytes and throughout the neuropil. The increase in apoE expression closely correlated in time and spatial distribution with axonal and neuronal degeneration as determined with a silver staining procedure, consistent with a role as an 'injury-response' protein.
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?
The observed statistical association supports continued evaluation of apoe as a potential injury-response protein in experimental studies of motor neuron degeneration.
“Our observed statistical association supports a continued evaluation of apoe as a potential “injury-response” protein in experimental studies of motor neuron degeneration (62).”
From Association of ALS with head injury, cigarette smoking and APOE genotypes (2010) · cites this paper as [62]
Citations
Cites
Fagan, A. M., Murphy, B. A., Patel, S. N., Kilbridge, J. F., Mobley, W. C., Bu, G., & Holtzman, D. M. (1998) · Experimental Neurology · doi:10.1006/exnr.1998.6818 · Cited by 116
Flagged first, then by citations
Research works printed but not linked: 16
- al-Chalabi, 1996, Association of apolipoprotein E epsilon 4 allele with bulbar-onset motor neuron disease, Lancet, 347, 159, 10.1016/S0140-6736(96)90343-8 · DOI · Paper page
- Bedlack, 2000, Apolipoprotein E and neuromuscular disease: a critical review of the literature, Arch. Neurol., 57, 1561, 10.1001/archneur.57.11.1561 · DOI
- Beffert, 1998, The neurobiology of apolipoproteins and their receptors in the CNS and Alzheimer's disease, Brain. Res. Rev., 27, 119, 10.1016/S0165-0173(98)00008-3 · DOI
- Boyles, 1989, A role for apolipoprotein E, apolipoprotein A-I, and low density lipoprotein receptors in cholesterol transport during regeneration and remyelination of the rat sciatic nerve, J. Clin. Invest., 83, 1015, 10.1172/JCI113943 · DOI · Paper page
- Grootendorst, 2000, Presence of apolipoprotein E immunoreactivity in degenerating neurones of mice is dependent on the severity of kainic acid-induced lesion, Brain Res., 868, 165, 10.1016/S0006-8993(00)02250-2 · DOI
- Gurney, 1994, Motor neuron degeneration in mice that express a human Cu, Zn superoxide dismutase mutation, Science, 264, 1772, 10.1126/science.8209258 · DOI · Paper page
- Herz, 2001, The LDL receptor gene family: (un)expected signal transducers in the brain, Neuron, 29, 571, 10.1016/S0896-6273(01)00234-3 · DOI
- Jaarsma, 2000, Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial degeneration, axonal degeneration and premature motoneuron death, and accelerates the development of motoneuron disease in mice expressing fALS-mutant SOD1, Neurobiol. Dis., 7, 623, 10.1006/nbdi.2000.0299 · DOI
- Jaarsma, 2001, CuZn superoxide dismutase (SOD1) accumulate in vacuolated mitochondria in transgenic mice expressing amyotrophic lateral sclerosis (ALS)-linked SOD1 mutations, Acta Neuropathol., 102, 293, 10.1007/s004010100399 · DOI
- Laskowitz, 1998, The CNS response to injury, J. Cereb. Blood Flow Metab., 18, 465, 10.1097/00004647-199805000-00001 · DOI · Paper page
- Moulard, 1996, Apolipoprotein E genotyping in sporadic amyotrophic lateral sclerosis: evidence for a major influence on the clinical presentation and prognosis, J. Neurol. Sci., 139, 34, 10.1016/0022-510X(96)00085-8 · DOI · Paper page
- Mui, 1995, Apolipoprotein E epsilon 4 allele is not associated with earlier age at onset in amyotrophic lateral sclerosis, Ann. Neurol., 38, 460, 10.1002/ana.410380318 · DOI
- Mulder, 1998, Increased apolipoprotein E expression in a transgenic mouse model for amyotrophic lateral sclerosis, Eur. J. Neurosci. (Suppl.), 10, 374
- Olsen, 2001, Disease mechanisms revealed by transcription profiling in SOD1-G93A transgenic mouse spinal cord, Ann. Neurol., 50, 730, 10.1002/ana.1252 · DOI
- Schauwecker, 1998, Differential regulation of astrocytic mRNAs in the rat striatum after lesions of the cortex or substantia nigra, Exp. Neurol., 149, 87, 10.1006/exnr.1997.6679 · DOI
- Smith, 1996, Apolipoprotein E epsilon 4 in bulbar-onset motor neuron disease, Lancet, 348, 334, 10.1016/S0140-6736(05)64502-3 · DOI · Paper page
Cited by
Sorted by citations
Cholesterol metabolism in neurons and astrocytes
Pfrieger, F. W., & Ungerer, N. (2011) · Progress in Lipid Research · doi:10.1016/j.plipres.2011.06.002 · Cited by 500
Association of ALS with head injury, cigarette smoking and APOE genotypes
Schmidt, S., Kwee, L. C., Allen, K. D., & Oddone, E. Z. (2010) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2010.01.011 · Cited by 117
Metadata
- Authors
- Haasdijk, E. D., Vlug, A., Mulder, M. T., & Jaarsma, D.
- Affiliations
- Erasmus University Rotterdam (NL)
- Maastricht University (NL)
- Corresponding author
- Jaarsma, Dick
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 2002-12
- Volume
- 335
- Issue
- 1
- Pages
- 29-33
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2009538497
- Cited by
- 29
- References
- 1
- Citations by year
- 2025: 1 · 2023: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 1 · 2013: 1 · 2012: 1
- FWCI
- 1.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Internal Medicine › Amyloidosis: Diagnosis, Treatment, Outcomes
- Keywords
- apolipoprotein E, amyotrophic lateral sclerosis, SOD1 G93A mice, spinal cord, neurodegeneration, astrocytes, axonal degeneration, injury response
- MeSH terms
- Amyotrophic Lateral Sclerosis, Animals, Apolipoproteins E, Astrocytes, Axons, Immunohistochemistry, Mice, Transgenic, Mutation, Nerve Degeneration, Neurons, Paralysis, Spinal Cord, Superoxide Dismutase, Blotting, Western, Neuropil, Mice
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