Neuronal migration depends on intact peroxisomal function in brain and in extraneuronal tissues
Open accessAbstract
Functional peroxisome deficiency, as encountered in Zellweger syndrome, causes a specific impairment of neuronal migration. Although the molecular mechanisms underlying the neuronal migration defect are at present unknown, the excess of very long chain fatty acids in brain, a consequence of peroxisomalbeta-oxidation deficiency, has often been hypothesized to play a major role. The purpose of the present study was to investigate the contribution of peroxisomal dysfunction in brain as opposed to peroxisomal dysfunction in extraneuronal tissues to the migration defect. Peroxisomes were selectively reconstituted either in brain or liver of Pex5 knock-out mice, a model for Zellweger syndrome, by tissue-selective overexpression of Pex5p. We found that both rescue strains exhibited a significant correction of the neuronal migration defect despite an incomplete reconstitution of peroxisomal function in the targeted tissue. Animals with a simultaneous rescue of peroxisomes in both tissues displayed a pattern of neuronal migration indistinguishable from that of wild-type animals on the basis of cresyl violet staining and 5',3'-bromo-2'-deoxyuridine birth-dating analysis. These data suggest that peroxisomal metabolism in brain but also in extraneuronal tissues affects the normal development of the mouse neocortex. In liver-rescued mice, the improvement of the neuronal migration was not accompanied by changes in very long chain fatty acid, docosahexaenoic acid, or plasmalogen levels in brain, indicating that other metabolic factors can influence the neuronal migration process.
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In Pex5-deficient mice (ubiquitous KO), liver-specific ectopic expression of Pex5 results in partial rescue of brain defects.
“This finding is further corroborated by observations in Pex5-deficient mice (ubiquitous KO), in which liver-specific ectopic expression of Pex5 [77] resulted in partial rescue of the brain defects.”
From Peroxisomes in brain development and function (2016) · cites this paper as [77]
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Eberhart, T., Charles, K. N., Salumbides-Torres, B., Price, N., Fliesler, S. J., Faust, P. L., & Kovacs, W. J. (2026) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2026.1636268 · Cited by 1 · see citing works
Raymond, G. V., Baranano, K. W., & Fatemi, A. S. (2012) · Elsevier eBooks · doi:10.1016/b978-1-4377-0435-8.00038-x · Cited by 1 · see citing works
Baarine, M. (2010) · theses.fr (ABES) · doi:10.70675/7ab2bcc8z16d2z420cz92f9zb3fd52371382 · Cited by 1 · see citing works
Mouse Models with Peroxisome Biogenesis Defects
Baes, M. I., Verheijden, S., & Veldhoven, P. P. V. (2014) · Springer eBooks · doi:10.1007/978-3-7091-1788-0_2
Passemard, S., Kaindl, A. M., Verche, V. L., Dournaud, P., & Gressèns, P. (2010) · Cambridge University Press eBooks · doi:10.1017/cbo9780511711848.006
ALTERED GLYCOLIPID METABOLISM AND ITS CELL BIOLOGICAL IMPACT IN PEROXISOMAL BIOGENESIS DISORDERS
宮崎, セ. (2014) · Institutional Repositories DataBase (IRDB) · doi:10.15083/00008996
Raymond, G. V. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-813955-4.00068-4
Lachman, R. S. (2007) · Elsevier eBooks · doi:10.1016/b978-0-323-01931-6.50034-7
Raymond, G. V. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-19041-4.00061-3
Peroxisomes: Organization and Transport in Neurons
Rayapuram, N., & Subramani, S. E. (2009) · Elsevier eBooks · doi:10.1016/b978-008045046-9.00735-x
Li, L. N., Zou, W., Lv, Y., Lu, Y., Liang, J., Zhang, S., Hu, B., & Jiao, J. (2026) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2600571123
- Authors
- Janssen, A., Gressens, P., Grabenbauer, M., Baumgart, E., Schad, A., Vanhorebeek, I., Brouwers, A., Declercq, P. E., Fahimi, D., Evrard, P., Schoonjans, L., Collen, D., Carmeliet, P., Mannaerts, G., Van Veldhoven, P., & Baes, M.
- Affiliations
- Heidelberg University (DE)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2003-10-29
- Volume
- 23
- Issue
- 30
- Pages
- 9732-9741
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6740889
- OpenAlex
- W2160464289
- Cited by
- 65
- References
- 43
- Citations by year
- 2026: 3 · 2024: 2 · 2023: 3 · 2022: 2 · 2021: 2 · 2020: 4 · 2019: 4 · 2018: 2 · 2017: 1 · 2015: 1 · 2014: 4 · 2013: 4 · 2012: 2
- FWCI
- 2.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- European Commission
- Vlaamse regering
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Fetal and Pediatric Neurological Disorders
- Keywords
- neuronal migration, peroxisomal dysfunction, Zellweger syndrome, very long chain fatty acids, peroxisomal beta-oxidation, neocortex development, liver, brain, docosahexaenoic acid, plasmalogens
- MeSH terms
- Peroxisome-Targeting Signal 1 Receptor, Animals, Brain, Bromodeoxyuridine, Cell Movement, Intermediate Filament Proteins, Liver, Mice, Transgenic, Nerve Tissue Proteins, Neurons, Organ Specificity, Phenotype, Gene Expression, Receptors, Cytoplasmic and Nuclear, Mice, Knockout, Peroxisomes, Mice, Nestin
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