ArticleASN neuro2010
Increased Plp1 gene expression leads to massive microglial cell activation and inflammation throughout the brain.
Article in ASN neuro, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 60 citations in OpenAlex.
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- Pathology of the neurovascular unit in leukodystrophies.Acta neuropathologica communications · 2021Article
- Spatiotemporal patterns of gene expression around implanted silicon electrode arrays.Journal of neural engineering · 2021Article
- Article
- The wmN1 Enhancer Region of the Mouse Myelin Proteolipid Protein Gene (mPlp1) is Indispensable for Expression of an mPlp1-lacZ Transgene in Both the CNS and PNS.Neurochemical research · 2020Article
- Innovative mouse model mimicking human-like features of spinal cord injury: efficacy of Docosahexaenoic acid on acute and chronic phases.Scientific reports · 2019Article
- Lipocalin-2 is a pathogenic determinant and biomarker of neuropsychiatric lupus.Journal of autoimmunity · 2019Article
- Oxidative stress and mitochondrial dynamics malfunction are linked in Pelizaeus-Merzbacher disease.Brain pathology (Zurich, Switzerland) · 2018Article
- Article
- Insertion of proteolipid protein into mitochondria but not DM20 regulates metabolism of cells.Neuroscience letters · 2018Article
- Protective Effect of Hyperbaric Oxygen on Cognitive Impairment Induced by D-Galactose in Mice.Neurochemical research · 2016Article
- Novel pathologic findings in patients with Pelizaeus-Merzbacher disease.Neuroscience letters · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
PMD (Pelizaeus-Merzbacher disease) is a rare neurodegenerative disorder that impairs motor and cognitive functions and is associated with a shortened lifespan. The cause of PMD is mutations of the PLP1 [proteolipid protein 1 gene (human)] gene. Transgenic mice with increased Plp1 [proteolipid protein 1 gene (non-human)] copy number model most aspects of PMD patients with duplications. Hypomyelination and demyelination are believed to cause the neurological abnormalities in mammals with PLP1 duplications. We show, for the first time, intense microglial reactivity throughout the grey and white matter of a transgenic mouse line with increased copy number of the native Plp1 gene. Activated microglia in the white and grey matter of transgenic mice are found as early as postnatal day 7, before myelin commences in normal cerebra. This finding indicates that degeneration of myelin does not cause the microglial response. Microglial numbers are doubled due to in situ proliferation. Compared with the jp (jimpy) mouse, which has much more oligodendrocyte death and hardly any myelin, microglia in the overexpressors show a more dramatic microglial reactivity than jp, especially in the grey matter. Predictably, many classical markers of an inflammatory response, including TNF-α (tumour necrosis factor-α) and IL-6, are significantly up-regulated manyfold. Because inflammation is believed to contribute to axonal degeneration in multiple sclerosis and other neurodegenerative diseases, inflammation in mammals with increased Plp1 gene dosage may also contribute to axonal degeneration described in patients and rodents with PLP1 increased gene dosage.
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