ReviewFrontiers in neuroscience2019
NeurodegenERation: The Central Role for ER Contacts in Neuronal Function and Axonopathy, Lessons From Hereditary Spastic Paraplegias and Related Diseases.
Review in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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.
The trial behind it
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
32 citing papers in PubMed, 54 citations in OpenAlex.
- Cerebellar deep brain stimulation rescues Purkinje cell mitochondrial density in a genetic mouse model of cerebellar ataxia.Brain research bulletin · 2026Article
- The Endoplasmic Reticulum and Its Contacts: Emerging Roles in Axon Development, Neurotransmission, and Degeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Article
- A genetic screen to uncover mechanisms underlying lipid transfer protein function at membrane contact sites.Life science alliance · 2024Article
- An Automated Imaging-Based Screen for Genetic Modulators of ER Organisation in Cultured Human Cells.Cells · 2024Article
- REEP1 Preserves Motor Function in SOD1Neuroscience bulletin · 2023Article
- Review
- Lunapark deficiency leads to an autosomal recessive neurodevelopmental phenotype with a degenerative course, epilepsy and distinct brain anomalies.Brain communications · 2023Article
- Case report: High-frequency repetitive transcranial magnetic stimulation for treatment of hereditary spastic paraplegia type 11.Frontiers in neurology · 2023Article
- TMEM63C mutations cause mitochondrial morphology defects and underlie hereditary spastic paraplegia.Brain : a journal of neurology · 2022Article
- Review
- Liver X receptor-agonist treatment rescues degeneration in a Drosophila model of hereditary spastic paraplegia.Acta neuropathologica communications · 2022Article
- TREX1 Deficiency Induces ER Stress-Mediated Neuronal Cell Death by Disrupting CaMolecular neurobiology · 2022Article
- Small Molecule Improvement of Trafficking Defects in Models of Neurodegeneration.ACS chemical neuroscience · 2021Article
- Implication of folate deficiency in CYP2U1 loss of function.The Journal of experimental medicine · 2021Article
- A novel automated image analysis pipeline for quantifying morphological changes to the endoplasmic reticulum in cultured human cells.BMC bioinformatics · 2021Article
- ER - lysosome contacts at a pre-axonal region regulate axonal lysosome availability.Nature communications · 2021Article
- Article
- Review
- Mind the Gap: Mitochondria and the Endoplasmic Reticulum in Neurodegenerative Diseases.Biomedicines · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hereditary spastic paraplegias (HSPs) are a group of inherited neurodegenerative conditions whose characteristic feature is degeneration of the longest axons within the corticospinal tract which leads to progressive spasticity and weakness of the lower limbs. Though highly genetically heterogeneous, the majority of HSP cases are caused by mutations in genes encoding proteins that are responsible for generating and organizing the tubular endoplasmic reticulum (ER). Despite this, the role of the ER within neurons, particularly the long axons affected in HSP, is not well understood. Throughout axons, ER tubules make extensive contacts with other organelles, the cytoskeleton and the plasma membrane. At these ER contacts, protein complexes work in concert to perform specialized functions including organelle shaping, calcium homeostasis and lipid biogenesis, all of which are vital for neuronal survival and may be disrupted by HSP-causing mutations. In this article we summarize the proteins which mediate ER contacts, review the functions these contacts are known to carry out within neurons, and discuss the potential contribution of disruption of ER contacts to axonopathy in HSP.
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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.