ArticleAnnals of translational medicine2021
Role of spindle pole body component 25 in neurodegeneration.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
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- Localised delivery of interleukin-13 from a PLGA microparticle embedded GelMA hydrogel improves functional and histopathological recovery in a mouse contusion spinal cord injury model.Bioactive materials · 2025Article
- Plasma proteomic Alzheimer's risk score: Biological age clock and pseudotime trajectory.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Berberine restrains non-small cell lung cancer cell growth, invasion and glycolysis via inactivating the SPC25/NUF2 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Cerebrospinal fluid proteomics identification of biomarkers for amyloid and tau PET stages.Cell reports. Medicine · 2025Article
- Novel floxed cannabinoid receptor 2 mouse line combines knockout capability with dual fluorescent reporters.Frontiers in pharmacology · 2025Article
- Systemic administration of novel engineered AAV capsids facilitates enhanced transgene expression in the macaque CNS.Med (New York, N.Y.) · 2023Article
- Combinational treatments of RNA interference and extracellular vesicles in the spinocerebellar ataxia.Frontiers in molecular neuroscience · 2022Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAberrant growth and polarization of microglia are critical for pathological initiation and progression of neurodegenerative conditions like Alzheimer's disease (AD). However, the molecular signals that govern the outgrowth of microglia have not yet been fully determined. Spindle pole body component 25 (SPC25) is an important part for forming NDC80 complex, which plays a key role in the assembly of the microtubule-binding domain of kinetochores. Nevertheless, the role of SPC25 in microglial growth during neurodegeneration has not been described before, and was thus addressed in the current study.
methodsWe generated an adeno-associated virus (AAV) serotype PHP.B carrying short hairpin RNA (shRNA) for SPC25 (shSPC25) under a microglia-specific TMEM119 promoter (AAV-pTMEM-shSPC25). Serotype PHP.B allowed the virus to cross blood-brain barrier, while TMEM119 promoter allowed specific targeting microglia in vitro and in vivo. We intravenously administrated AAV-pTMEM-shSPC25 to AD-prone APP/PS1 male and female mice and determined this effect on microglia proliferation and mouse behavior.
resultsDepletion of SPC25 did not alter polarization of microglia cell polarization in vitro. On the other hand, AD-prone APP/PS1 mice that had received AAV-pTMEM-shSPC25 significantly decreased SPC25 levels in microglia and attenuated microglia proliferation, resulting in significant improvement of the performance of the mice in behavior tests.
conclusionsSpecific depletion of SPC25 in microglia may prevent AD development through suppression of microglia outgrowth. SPC25 may be a promising novel target for preventing AD through microglia.
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