ArticleFrontiers in cellular neuroscience2019
SNX8 Enhances Non-amyloidogenic APP Trafficking and Attenuates Aβ Accumulation and Memory Deficits in an AD Mouse.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Long Non-Coding RNAs and Alzheimer's Disease: Towards Personalized Diagnosis.International journal of molecular sciences · 2024Article
- SNX8 enables lysosome reformation and reverses lysosomal storage disorder.Nature communications · 2024Article
- A set of common buccal CpGs that predict epigenetic age and associate with lifespan-regulating genes.iScience · 2022Article
- The tyrosine kinase inhibitor LPM4870108 impairs learning and memory and induces transcriptomic and gene‑specific DNA methylation changes in rats.Archives of toxicology · 2022Article
- Identification of the protective effect ofPharmaceutical biology · 2021Article
- Article
- Sorting Out Sorting Nexins Functions in the Nervous System in Health and Disease.Molecular neurobiology · 2021Review
- Enhancing α-secretase Processing for Alzheimer's Disease-A View on SFRP1.Brain sciences · 2020Article
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Dysregulation of various APP trafficking components in the endosome has been previously implicated in Alzheimer's disease (AD). Although single nucleotide polymorphisms within the gene locus encoding the endosomal component, SNX8 have been previously associated with AD, how SNX8 levels are altered and its contribution to AD onset is currently unknown. Here, we observe decreased expression of SNX8 in human AD and AD mouse brain. SNX8 predominantly localized to early and late endosomes, where SNX8 overexpression enhanced total APP levels, cell surface APP distribution and consequent soluble APPα cleavage. SNX8 depletion resulted in elevated β-amyloid (Aβ) levels, while SNX8 overexpression reduced Aβ levels in cells and in an APP/PS1 AD mouse model. Importantly, SNX8 overexpression rescued cognitive impairment in APP/PS1 mice. Together, these results implicate a neuroprotective role for SNX8 in enhancing non-amyloidogenic APP trafficking and processing pathways. Given that endosomal dysfunction is an early event in AD, restoration of dysfunctional endosomal components such as SNX8 may be beneficial in future therapeutic strategies.
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