ArticleCerebellum (London, England)2014
Torpedo formation and Purkinje cell loss: modeling their relationship in cerebellar disease.
Article in Cerebellum (London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pathophysiology of Cerebellar Tremor: The Forward Model-Related Tremor and the Inferior Olive Oscillation-Related Tremor.Frontiers in neurology · 2021Pooled it
- Oligodendrocyte dysfunction contributes to motor deficits and Purkinje cell axonopathy in spinocerebellar ataxia type 1.The Journal of clinical investigation · 2026Article
- Characterization of cerebellar amyloid-β deposits in Alzheimer disease.Journal of neuropathology and experimental neurology · 2024Article
- Early-onset familial essential tremor is associated with nucleotide expansions of spinocerebellar ataxia in China.Molecular biology reports · 2024Article
- Increased understanding of complex neuronal circuits in the cerebellar cortex.Frontiers in cellular neuroscience · 2024Review
- Pharmacological inhibition of FABP7 by MF 6 counteracts cerebellum dysfunction in an experimental multiple system atrophy mouse model.Acta pharmacologica Sinica · 2024Article
- Gene Expression Analysis of Laser-Captured Purkinje Cells in the Essential Tremor Cerebellum.Cerebellum (London, England) · 2023Article
- Visuomotor Adaptation Deficits in Patients with Essential Tremor.Cerebellum (London, England) · 2023Article
- Histopathology of the cerebellar cortex in essential tremor and other neurodegenerative motor disorders: comparative analysis of 320 brains.Acta neuropathologica · 2023Article
- Myelinating Glia: Potential Therapeutic Targets in Polyglutamine Spinocerebellar Ataxias.Cells · 2023Review
- A rad50 germline mutation induces tumorigenesis and ataxia-telangiectasia phenotype in a transparent medaka model.PloS one · 2023Article
- Is essential tremor a degenerative disorder or an electric disorder? Degenerative disorder.International review of neurobiology · 2022Article
- Paranodal Axoglial Junctions, an Essential Component in Axonal Homeostasis.Frontiers in cell and developmental biology · 2022Review
- Purkinje cell axonal swellings enhance action potential fidelity and cerebellar function.Nature communications · 2021Article
- Human alpha-synuclein overexpressing MBP29 mice mimic functional and structural hallmarks of the cerebellar subtype of multiple system atrophy.Acta neuropathologica communications · 2021Article
- Tau Protein Phosphorylated at Threonine-231 is Expressed Abundantly in the Cerebellum in Prion Encephalopathies.Journal of Alzheimer's disease : JAD · 2021Article
- Essential Tremor Within the Broader Context of Other Forms of Cerebellar Degeneration.Cerebellum (London, England) · 2020Review
- Essential tremor pathology: neurodegeneration and reorganization of neuronal connections.Nature reviews. Neurology · 2020Review
- The proteasome regulator PI31 is required for protein homeostasis, synapse maintenance, and neuronal survival in mice.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Contextualizing the pathology in the essential tremor cerebellar cortex: a patholog-omics approach.Acta neuropathologica · 2019Article
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Authors and funding
4 authors.
Funding
Abstract
Torpedo formation and Purkinje cell (PC) loss represent standard and inter-related cerebellar responses to injury. Surprisingly, the nature of their relationship has not been carefully characterized across a range of normal and disease states. Are brains with more torpedoes expected to have fewer PCs? We quantified torpedoes and PCs in four groups: essential tremor (ET), spinocerebellar ataxia (SCA), multiple system atrophy-cerebellar (MSA-C), and controls. Brains from 100 individuals (58 ET, 27 controls, 7 SCA, 8 MSA-C) were available at the New York Brain Bank. After complete neuropathological assessment, a standard parasagittal neocerebellar block was harvested; a 7-μm thick section was stained with Luxol fast blue/hematoxylin and eosin; and torpedoes and PCs were quantified. For a given PC count, SCA and MSA-C cases often had higher torpedo counts than ET cases or controls. Furthermore, the relationship between torpedo and PC counts was complex. The correlation between torpedo and PC counts was negative in ET cases (i.e., individuals with more torpedoes had fewer PCs [i.e., more PC loss]) whereas the relationship was positive in MSA-C cases (i.e., individuals with fewer PCs [i.e., more PC loss] had fewer torpedoes). Patients with SCA showed both patterns. When all diagnostic groups were combined, the correlation was best fit by a quadratic (i.e., parabolic) model rather than a simple linear model; this model incorporated data on the negative correlation in ET cases, the mixed results in SCA cases, and the positive correlation in MSA-C cases (r = 0.636). The relationship between torpedo and PC counts was complex and heterogeneous across a range of cerebellar disease states, and was best characterized by a quadratic rather than a simple model. With more severe cerebellar disease, torpedoes can be quite numerous and are likely a common feature of surviving PCs, but eventually, dramatic loss of PC leads to a paradoxical reduction in observable torpedoes.
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