ReviewActa neuropathologica communications2014
Lipid dysfunction and pathogenesis of multiple system atrophy.
Review in Acta neuropathologica communications, 2014. 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, 48 citations in OpenAlex.
- Cellular and systemic modifiers of alpha-synuclein proteostasis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- The role of alpha-synuclein in synucleinopathy: Impact on lipid regulation at mitochondria-ER membranes.NPJ Parkinson's disease · 2025Article
- Lipids and α-Synuclein: adding further variables to the equation.Frontiers in molecular biosciences · 2024Review
- Coenzyme Q10: A Biomarker in the Differential Diagnosis of Parkinsonian Syndromes.Antioxidants (Basel, Switzerland) · 2023Article
- Multiple system atrophy: at the crossroads of cellular, molecular and genetic mechanisms.Nature reviews. Neuroscience · 2023Review
- Early and extensive alterations of glial connexins, distal oligodendrogliopathy type demyelination, and nodal/paranodal pathology are characteristic of multiple system atrophy.Brain pathology (Zurich, Switzerland) · 2023Article
- Neuropathology of SCA34 showing widespread oligodendroglial pathology with vacuolar white matter degeneration: a case study.Acta neuropathologica communications · 2021Article
- Investigating ELOVL7 coding variants in multiple system atrophy.Neuroscience letters · 2021Article
- Vesicle trafficking and lipid metabolism in synucleinopathy.Acta neuropathologica · 2021Review
- Association of mitochondrial genomic background with risk of Multiple System Atrophy.Parkinsonism & related disorders · 2020Article
- An update on MSA: premotor and non-motor features open a window of opportunities for early diagnosis and intervention.Journal of neurology · 2020Review
- Multiple system atrophy - a clinicopathological update.Free neuropathology · 2020Article
- Neuropathology and pathogenesis of extrapyramidal movement disorders: a critical update-I. Hypokinetic-rigid movement disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
- Understanding the pathogenesis of multiple system atrophy: state of the art and future perspectives.Acta neuropathologica communications · 2019Review
- Assessment of APOE in atypical parkinsonism syndromes.Neurobiology of disease · 2019Article
- Converging Patterns of α-Synuclein Pathology in Multiple System Atrophy.Journal of neuropathology and experimental neurology · 2018Article
- Multiple system atrophy and apolipoprotein E.Movement disorders : official journal of the Movement Disorder Society · 2018Article
- Multiple System Atrophy: An Oligodendroglioneural Synucleinopathy1.Journal of Alzheimer's disease : JAD · 2018Review
- Multiple system atrophy: experimental models and reality.Acta neuropathologica · 2018Review
- Progression of alpha-synuclein pathology in multiple system atrophy of the cerebellar type.Neuropathology and applied neurobiology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by the accumulation of α-synuclein protein in the cytoplasm of oligodendrocytes, the myelin-producing support cells of the central nervous system (CNS). The brain is the most lipid-rich organ in the body and disordered metabolism of various lipid constituents is increasingly recognized as an important factor in the pathogenesis of several neurodegenerative diseases. α-Synuclein is a 17 kDa protein with a close association to lipid membranes and biosynthetic processes in the CNS, yet its precise function is a matter of speculation, particularly in oligodendrocytes. α-Synuclein aggregation in neurons is a well-characterized feature of Parkinson's disease and dementia with Lewy bodies. Epidemiological evidence and in vitro studies of α-synuclein molecular dynamics suggest that disordered lipid homeostasis may play a role in the pathogenesis of α-synuclein aggregation. However, MSA is distinct from other α-synucleinopathies in a number of respects, not least the disparate cellular focus of α-synuclein pathology. The recent identification of causal mutations and polymorphisms in COQ2, a gene encoding a biosynthetic enzyme for the production of the lipid-soluble electron carrier coenzyme Q10 (ubiquinone), puts membrane transporters as central to MSA pathogenesis, although how such transporters are involved in the early myelin degeneration observed in MSA remains unclear. The purpose of this review is to bring together available evidence to explore the potential role of membrane transporters and lipid dyshomeostasis in the pathogenesis of α-synuclein aggregation in MSA. We hypothesize that dysregulation of the specialized lipid metabolism involved in myelin synthesis and maintenance by oligodendrocytes underlies the unique neuropathology of MSA.
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