ArticleMolecular genetics and metabolism2015
Pallidal neuronal apolipoprotein E in pantothenate kinase-associated neurodegeneration recapitulates ischemic injury to the globus pallidus.
Article in Molecular genetics and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Deletion of Robo4 worsens neuroinflammation in a mouse model of Alzheimer's disease.Physiological reports · 2026Article
- Acidosis, Iron Dyshomeostasis and Inflammatory Injury.International journal of molecular sciences · 2026Review
- Lower cerebral blood flow but not cerebrovascular response in elastin haploinsufficient mice.Experimental physiology · 2026Article
- Apolipoprotein E Gene Polymorphism Effects on Lipid Metabolism and Risk of Cerebral Infarction in Northwest Han Chinese Population.Pharmacogenomics and personalized medicine · 2023Article
- PKAN pathogenesis and treatment.Molecular genetics and metabolism · 2022Review
- Cognitive and Physical Intervention in Metals' Dysfunction and Neurodegeneration.Brain sciences · 2022Review
- Proton magnetic resonance spectroscopy detects cerebral metabolic derangement in a mouse model of brain coenzyme a deficiency.Journal of translational medicine · 2022Article
- Coenzyme a Biochemistry: From Neurodevelopment to Neurodegeneration.Brain sciences · 2021Review
- Mitochondrial Dysfunction, Oxidative Stress and Neuroinflammation in Neurodegeneration with Brain Iron Accumulation (NBIA).Antioxidants (Basel, Switzerland) · 2020Review
- A pantothenate kinase-deficient mouse model reveals a gene expression program associated with brain coenzyme a reduction.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- 4'-Phosphopantetheine corrects CoA, iron, and dopamine metabolic defects in mammalian models of PKAN.EMBO molecular medicine · 2019Article
- Neuropathology and pathogenesis of extrapyramidal movement disorders: a critical update. II. Hyperkinetic disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
- Proposed Therapies for Pantothenate-Kinase-Associated Neurodegeneration.Journal of experimental neuroscience · 2019Article
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
Pantothenate kinase-associated neurodegeneration (PKAN) is a progressive movement disorder that is due to mutations in PANK2. Pathologically, it is a member of a class of diseases known as neurodegeneration with brain iron accumulation (NBIA) and features increased tissue iron and ubiquitinated proteinaceous aggregates in the globus pallidus. We have previously determined that these aggregates represent condensed residue derived from degenerated pallidal neurons. However, the protein content, other than ubiquitin, of these aggregates remains unknown. In the present study, we performed biochemical and immunohistochemical studies to characterize these aggregates and found them to be enriched in apolipoprotein E that is poorly soluble in detergent solutions. However, we did not determine a significant association between APOE genotype and the clinical phenotype of disease in our database of 81 cases. Rather, we frequently identified similar ubiquitin- and apolipoprotein E-enriched lesions in these neurons in non-PKAN patients in the penumbrae of remote infarcts that involve the globus pallidus, and occasionally in other brain sites that contain large γ-aminobutyric acid (GABA)ergic neurons. Our findings, taken together, suggest that tissue or cellular hypoxic/ischemic injury within the globus pallidus may underlie the pathogenesis of PKAN.
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