ArticleJournal of molecular neuroscience : MN2015
Short-term cuprizone feeding verifies N-acetylaspartate quantification as a marker of neurodegeneration.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Polyphenon E, non-futile at neuroprotection in multiple sclerosis but unpredictably hepatotoxic: Phase I single group and phase II randomized placebo-controlled studies.Journal of the neurological sciences · 2015Trial
- Oligodendrocyte Lineage Marker Expression in eGFP-GFAP Transgenic Mice.Journal of molecular neuroscience : MN · 2021Article
- The Cuprizone Model: Dos and Do Nots.Cells · 2020Review
- Diverse Gene Expressions in the Prediction of Cuprizone-Induced Demyelination.Neurotoxicity research · 2020Article
- Mitochondrial Impairment in Oligodendroglial Cells Induces Cytokine Expression and Signaling.Journal of molecular neuroscience : MN · 2019Article
- Oncogenic features of neuromedin U in breast cancer are associated with NMUR2 expression involving crosstalk with members of the WNT signaling pathway.Oncotarget · 2017Article
- Thalamus Degeneration and Inflammation in Two Distinct Multiple Sclerosis Animal Models.Journal of molecular neuroscience : MN · 2016Article
- Lesion Expansion in Experimental Demyelination Animal Models and Multiple Sclerosis Lesions.Molecular neurobiology · 2016Article
- Absence of CCL2 and CCL3 Ameliorates Central Nervous System Grey Matter But Not White Matter Demyelination in the Presence of an Intact Blood-Brain Barrier.Molecular neurobiology · 2016Article
- Anatomical Distribution of Cuprizone-Induced Lesions in C57BL6 Mice.Journal of molecular neuroscience : MN · 2015Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proton magnetic resonance spectroscopy (1H-MRS) is a quantitative MR imaging technique often used to complement conventional MR imaging with specific metabolic information. A key metabolite is the amino acid derivative N-Acetylaspartate (NAA) which is an accepted marker to measure the extent of neurodegeneration in multiple sclerosis (MS) patients. NAA is catabolized by the enzyme aspartoacylase (ASPA) which is predominantly expressed in oligodendrocytes. Since the formation of MS lesions is paralleled by oligodendrocyte loss, NAA might accumulate in the brain, and therefore, the extent of neurodegeneration might be underestimated. In the present study, we used the well-characterized cuprizone model. There, the loss of oligodendrocytes is paralleled by a reduction in ASPA expression and activity as demonstrated by genome-wide gene expression analysis and enzymatic activity assays. Notably, brain levels of NAA were not increased as determined by gas chromatography-mass spectrometry and 1H-MRS. These important findings underpin the reliability of NAA quantification as a valid marker for the paraclinical determination of the extent of neurodegeneration, even under conditions of oligodendrocyte loss in which impaired metabolization of NAA is expected. Future studies have to reveal whether other enzymes are able to metabolize NAA or whether an excess of NAA is cleared by other mechanisms rather than enzymatic metabolism.
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