ArticleActa neuropathologica2017
Climbing fiber-Purkinje cell synaptic pathology in tremor and cerebellar degenerative diseases.
Article in Acta neuropathologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed.
- Neurophysiological Basis of Tremor Disorders: Parkinson's Disease, Essential Tremor, Tremor in Dystonia, and Holmes Tremor.Seminars in neurology · 2026Review
- Neuroprotection Across Cerebellar and Nigrostriatal Degeneration: Translational Insights from Parkinson's Disease to Spinocerebellar Ataxia Type 2.Cerebellum (London, England) · 2026Review
- Essential Tremor Cases with Subtle Cerebellar Pathology: A Systematic Study of Postmortem Cerebellar Changes.Cerebellum (London, England) · 2026Article
- Purkinje Cell Loss in Essential Tremor: Collective Data From 215 Brains Over a 21-Year Period.Annals of clinical and translational neurology · 2026Article
- The cerebellum shapes motions by encoding motor frequencies with precision and cross-individual uniformity.Nature biomedical engineering · 2025Article
- Loss-of-function variations in solute carrier family 38 member 6 are associated with essential tremor.Signal transduction and targeted therapy · 2025Article
- Fingolimod Prevents Neuroinflammation but Has a Limited Effect on the Development of Ataxia in a Mouse Model for SCA1.International journal of molecular sciences · 2025Article
- Clinical Heterogeneity of Essential Tremor: Understanding Neural Substrates of Action Tremor Subtypes.Cerebellum (London, England) · 2024Review
- Early-onset familial essential tremor is associated with nucleotide expansions of spinocerebellar ataxia in China.Molecular biology reports · 2024Article
- Tremor-associated short tandem repeat intermediate and pathogenic expansions in familial essential tremor.Brain communications · 2024Article
- Article
- Linking the cerebellum to Parkinson disease: an update.Nature reviews. Neurology · 2023Review
- Cerebellar and cerebral white matter changes in Parkinson's disease with resting tremor.Neuroradiology · 2023Article
- Physiological Recordings of the Cerebellum in Movement Disorders.Cerebellum (London, England) · 2023Review
- Early molecular layer interneuron hyperactivity triggers Purkinje neuron degeneration in SCA1.Neuron · 2023Article
- Genetic Deletion of Thorase Causes Purkinje Cell Loss and Impaired Motor Coordination Behavior.Cells · 2023Article
- Pre-ataxic loss of intrinsic plasticity and motor learning in a mouse model of SCA1.Brain : a journal of neurology · 2023Article
- Histopathology of the cerebellar cortex in essential tremor and other neurodegenerative motor disorders: comparative analysis of 320 brains.Acta neuropathologica · 2023Article
- Surgeon experience in glioblastoma surgery of the elderly-a multicenter, retrospective cohort study.Journal of neuro-oncology · 2023Article
- A review on pathology, mechanism, and therapy for cerebellum and tremor in Parkinson's disease.NPJ Parkinson's disease · 2022Review
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11 authors.
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Abstract
Changes in climbing fiber-Purkinje cell (CF-PC) synaptic connections have been found in the essential tremor (ET) cerebellum, and these changes are correlated with tremor severity. Whether these postmortem changes are specific to ET remains to be investigated. We assessed CF-PC synaptic pathology in the postmortem cerebellum across a range of degenerative movement disorders [10 Parkinson's disease (PD) cases, 10 multiple system atrophy (MSA) cases, 10 spinocerebellar ataxia type 1 (SCA1) cases, and 20 ET cases] and 25 controls. We observed differences in terms of CF pathological features across these disorders. Specifically, PD cases and ET cases both had more CFs extending into the parallel fiber (PF) territory, but ET cases had more complex branching and increased length of CFs in the PF territory along with decreased CF synaptic density compared to PD cases. MSA cases and SCA1 cases had the most severely reduced CF synaptic density and a marked paucity of CFs extending into the PF territory. Furthermore, CFs in a subset of MSA cases formed collateral branches parallel to the PC layer, a feature not seen in other diagnostic groups. Using unsupervised cluster analysis, the cases and controls could all be categorized into four clusters based on the CF pathology and features of PC pathology, including counts of PCs and their axonal torpedoes. ET cases and PD cases co-segregated into two clusters, whereas SCA1 cases and MSA cases formed another cluster, separate from the control cluster. Interestingly, the presence of resting tremor seemed to be the clinical feature that separated the cases into the two ET-PD clusters. In conclusion, our study demonstrates that these degenerative movement disorders seem to differ with respect to the pattern of CF synaptic pathology they exhibit. It remains to be determined how these differences contribute to the clinical presentations of these diseases.
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