ArticleFrontiers in cell and developmental biology2020
Upregulation of Prickle2 Ameliorates Alzheimer's Disease-Like Pathology in a Transgenic Mouse Model of Alzheimer's Disease.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Retrotransposon Expression Is Upregulated in Adulthood and Suppressed during Regeneration of the Limb in the Axolotl (Ambystoma mexicanum).Advanced biology · 2025Article
- Evolving Insights into Prickle2 in Neurodevelopment and Neurological Disorders.Molecular neurobiology · 2025Review
- Decoding Epilepsy: Prickle2 and Multifaceted Molecular Pathway Connections.Current pharmaceutical design · 2025Review
- The role of prickle proteins in vertebrate development and pathology.Molecular and cellular biochemistry · 2024Review
- Conserved gene signatures shared amongFrontiers in molecular biosciences · 2023Article
- Nucleosome assembly protein 1-like 5 alleviates Alzheimer's disease-like pathological characteristics in a cell model.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
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Abstract
Alzheimer's disease (AD) is a devastating neurodegenerative disorder that has no effective therapies. Prickle planar cell polarity protein 2 (Prickle2), is an important cytoplasmic regulator of Wnt/PCP signaling. It has been reported that Prickle2 deficiency reduced neurite outgrowth levels in mouse N2a cells and led to autism-like behaviors and hippocampal synaptic dysfunction in mice. However, much less is known about the relationship of Prickle2 to AD pathogenesis. RT-qPCR, Western blot and IHC results showed that the mRNA and protein levels of Prickle2 were reduced in APP/PS1/Tau transgenic (3xTg) mice. Intravenous injection of Prickle2-overexpressing AAV-PHP.eB vectors improved the cognitive deficits in 3xTg mice. We also demonstrated that Prickle2 could repress oxidative stress and neuroinflammation, ameliorate the amyloid β (Aβ) plaque pathology and reduce Tau hyperphosphorylation in APP/PS1 mice. Further investigation of the mechanism of Prickle2 in AD revealed that Prickle2 inhibited Wnt/PCP/JNK pathway in vivo and in vitro. Our results suggest that Prickle2 might be a potential candidate for the diagnosis and treatment of AD.
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