ArticleCNS neuroscience & therapeutics2025
DNLA Delayed the Appearance of Learning and Memory Impairment of APP/PS1 Mice: Involvement of mTOR/TFEB/v-ATPase Signaling Pathway.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Circ_0092222 is Enhanced in Alzheimer's Disease and Exacerbates Aβ-induced Neurotoxicity Through Sponging miR-331-3p.Molecular neurobiology · 2026Article
- Alkaloids from Dendrobium Nobile Lindl Improves Mitochondrial Function by Enhancing the Activity of v-ATPase in APP/PS1 Mice.Neurochemical research · 2026Article
- Cry2 deficiency leads to cognitive impairment through the microbiota-gut-brain axis mediated S1P/NLRP3/IL-1β pathway in mice.Journal of neuroinflammation · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
introductionAlzheimer's disease (AD) is a progressive neurodegenerative disorder with cognitive impairment that currently is incurable. There is existing evidence to suggest that vacuolar adenosine triphosphatase (v-ATPase) is one of the early key driving factors in the pathological process of AD. Thus, early intervention of v-ATPase may be a viable strategy.
aimsObserving whether early intervention with DNLA can delay learning and memory impairment in mice, and further exploring the mechanism of DNLA delaying AD in vitro based on v-ATPase.
methodsFour-month-old APP/PS1 transgenic mice were treated with alkaloids from Dendrobium nobile Lindl (DNLA) 20 and 40 mg/kg/day for 5 months. The Morris water maze test and nest test showed that DNLA administration significantly delayed the appearance of cognitive deficits in APP/PS1 mice. We further investigated the mechanism of DNLA promoting lysosome acidification in vitro by using PC12 cells.
resultsWe found that DNLA increases the degradation of β-amyloid (Aβ) contained in the autophagic lysosomes and alleviates the aging of neurons by promoting lysosome acidification and improving autophagy flow. In PC12 cells, DDB could promote the separation of mTOR and lysosome, promote the nuclear translocation of transcription factor EB (TFEB), and then promote lysosome biogenesis and lysosome acidification by targeting ATP6V1A.
conclusionThese results unraveled that preventive administration of DNLA may delay the impairment of learning and memory in APP/PS1 mice. The molecular mechanism may be related to promoting the mTOR-TFEB-v-ATPase pathway.
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