ArticleGlia2010
Altered levels and distribution of amyloid precursor protein and its processing enzymes in Niemann-Pick type C1-deficient mouse brains.
Article in Glia, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 54 citations in OpenAlex.
- Cholesterol crystal formation and embolism in the central nervous system and their potential role in Alzheimer's disease.American heart journal plus : cardiology research and practice · 2026Article
- Miglustat in Alzheimer's Disease Associated With Heterozygous NPC1 Mutation: Exploratory Case Series and Preliminary Findings.European journal of neurology · 2025Article
- Article
- Comparative Hippocampal Proteome and Phosphoproteome in a Niemann-Pick, Type C1 Mouse Model Reveal Insights into Disease Mechanisms.Journal of proteome research · 2024Article
- Reexamining the Causes and Effects of Cholesterol Deposition in the Brains of Patients with Alzheimer's Disease.Molecular neurobiology · 2023Review
- The role of DHCR24 in the pathogenesis of AD: re-cognition of the relationship between cholesterol and AD pathogenesis.Acta neuropathologica communications · 2022Review
- Implications of exosomes derived from cholesterol-accumulated astrocytes in Alzheimer's disease pathology.Disease models & mechanisms · 2021Article
- Identification of Novel Pathways Associated with Patterned Cerebellar Purkinje Neuron Degeneration in Niemann-Pick Disease, Type C1.International journal of molecular sciences · 2019Article
- Kainate Receptor Activation Enhances Amyloidogenic Processing of APP in Astrocytes.Molecular neurobiology · 2019Article
- The sterol regulatory element-binding protein 2 is dysregulated by tau alterations in Alzheimer disease.Brain pathology (Zurich, Switzerland) · 2019Article
- Hepatic and neuronal phenotype of NPC1Heliyon · 2019Article
- A role for astrocyte-derived amyloid β peptides in the degeneration of neurons in an animal model of temporal lobe epilepsy.Brain pathology (Zurich, Switzerland) · 2019Article
- Endosomal-Lysosomal Cholesterol Sequestration by U18666A Differentially Regulates Amyloid Precursor Protein (APP) Metabolism in Normal and APP-Overexpressing Cells.Molecular and cellular biology · 2018Article
- BACE1-cleavage of Sez6 and Sez6L is elevated in Niemann-Pick type C disease mouse brains.PloS one · 2018Article
- Astrocytes and lysosomal storage diseases.Neuroscience · 2016Review
- APP overexpression in the absence of NPC1 exacerbates metabolism of amyloidogenic proteins of Alzheimer's disease.Human molecular genetics · 2015Article
- Neuronal-Targeted TFEB Accelerates Lysosomal Degradation of APP, Reducing Aβ Generation and Amyloid Plaque Pathogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Lysosomal Storage Diseases-Regulating Neurodegeneration.Journal of experimental neuroscience · 2015Review
- The role of cholesterol metabolism in Alzheimer's disease.Molecular neurobiology · 2015Review
- Metals and cholesterol: two sides of the same coin in Alzheimer's disease pathology.Frontiers in aging neuroscience · 2014Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Niemann-Pick type C (NPC) disease is an autosomal recessive neurodegenerative disorder characterized by intracellular accumulation of cholesterol and glycosphingolipids in many tissues including the brain. The disease is caused by mutations of either NPC1 or NPC2 gene and is accompanied by a severe loss of neurons in the cerebellum, but not in the hippocampus. NPC pathology exhibits some similarities with Alzheimer's disease, including increased levels of amyloid beta (Abeta)-related peptides in vulnerable brain regions, but very little is known about the expression of amyloid precursor protein (APP) or APP secretases in NPC disease. In this article, we evaluated age-related alterations in the level/distribution of APP and its processing enzymes, beta- and gamma-secretases, in the hippocampus and cerebellum of Npc1(-/-) mice, a well-established model of NPC pathology. Our results show that levels and expression of APP and beta-secretase are elevated in the cerebellum prior to changes in the hippocampus, whereas gamma-secretase components are enhanced in both brain regions at the same time in Npc1(-/-) mice. Interestingly, a subset of reactive astrocytes in Npc1(-/-) mouse brains expresses high levels of APP as well as beta- and gamma-secretase components. Additionally, the activity of beta-secretase is enhanced in both the hippocampus and cerebellum of Npc1(-/-) mice at all ages, while the level of C-terminal APP fragments is increased in the cerebellum of 10-week-old Npc1(-/-) mice. These results, taken together, suggest that increased level and processing of APP may be associated with the development of pathology and/or degenerative events observed in Npc1(-/-) mouse brains.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.