Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Inhibiting mitochondrial fission rescues degeneration in hereditary spastic paraplegia neurons.

Brain : a journal of neurology - 21 Nov 2022

Chen Zhenyu, Chai Eric, Mou Yongchao, Roda Ricardo H, Blackstone Craig, Li Xue-Jun

Abstract excerpt

Hereditary spastic paraplegias are characterized by lower limb spasticity resulting from degeneration of long corticospinal axons. SPG11 is one of the most common autosomal recessive hereditary spastic paraplegias, and the SPG11 protein spatacsin forms a complex with the SPG15 protein spastizin and heterotetrameric AP5 adaptor protein complex, which includes the SPG48 protein AP5Z1. Using the integration-free...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adenosine Triphosphate
Share to Mitochondrial Dynamics

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mutation

Share to Neurons

Share to Proteins

Share to Spastic Paraplegia, Hereditary

Source

Open in PubMed Open full text

Identifiers

PMID: 35026838
DOI: 10.1093/brain/awab488
PMCID: PMC10200290

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inhibiting mitochondrial fission rescues degeneration in hereditary spastic paraplegia neurons.PMID 35026838Read ↗

Impaired mitochondrial dynamics underlie axonal defects in hereditary spastic paraplegias.Semantic proximity Read ↗

Oxidative Stress-Induced Axon Fragmentation Is a Consequence of Reduced Axonal Transport in Hereditary Spastic Paraplegia SPAST Patient NeuronsSemantic proximity Read ↗

Loss of spastin function results in disease-specific axonal defects in human pluripotent stem cell-based models of hereditary spastic paraplegia.Semantic proximity Read ↗

Rescue axonal defects by targeting mitochondrial dynamics in hereditary spastic paraplegiasSemantic proximity Read ↗

Pharmacologic rescue of axon growth defects in a human iPSC model of hereditary spastic paraplegia SPG3A.Semantic proximity Read ↗

Reversing Autophagy Inhibition Ameliorates Neurodegeneration in Hereditary Spastic Paraplegia Caused by a Degradation-Resistant SPAST Mutation.Semantic proximity Read ↗

Mitochondrial Function in Hereditary Spastic Paraplegia: Deficits in SPG7 but Not SPAST Patient-Derived Stem CellsSemantic proximity Read ↗

A reduction in Drp1-mediated fission compromises mitochondrial health in autosomal recessive spastic ataxia of Charlevoix SaguenaySemantic proximity Read ↗

Gene dosage-dependent rescue of HSP neurite defects in SPG4 patients' neuronsSemantic proximity Read ↗

Liver-X-receptor agonists rescue axonal degeneration in SPG11-deficient neurons via regulating cholesterol trafficking.Semantic proximity Read ↗

Converging cellular themes for the hereditary spastic paraplegias.Semantic proximity Read ↗

Genotype–Phenotype Distinctions in Spastic Paraplegia 4 Reveal HDAC6 as a Therapeutic TargetSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.