ArticleMolecular medicine reports2021
Nogo‑66 promotes β‑amyloid protein secretion via NgR/ROCK‑dependent BACE1 activation.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- RhoA in postnatal spinal motoneuron is essential for peripheral myelination.Communications biology · 2026Article
- A Novel Nogo-A Receptor Antagonist Peptide Impedes Alzheimer's Disease Pathology by Nogo-A/NgR/ROCK Signaling Pathway.CNS neuroscience & therapeutics · 2026Article
- Genome-wide pleiotropy analysis of longitudinal blood pressure and harmonized cognitive performance measures.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Analyses of Nogo-Family Genes in Mouse and Human Microglia Omics Datasets IdentifyCurrent neuropharmacology · 2025Article
- Critical role of ROCK1 in AD pathogenesis via controlling lysosomal biogenesis and acidification.Translational neurodegeneration · 2024Article
- Modeling the early stages of Alzheimer's disease by administering intracerebroventricular injections of human native Aβ oligomers to rats.Acta neuropathologica communications · 2022Article
- The Clinical Significance of Cerebrospinal Fluid Reticulon 4 (RTN4) Levels in the Differential Diagnosis of Neurodegenerative Diseases.Journal of clinical medicine · 2021Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The generation of β‑amyloid protein (Aβ) is considered a key step in the pathogenesis of Alzheimer's disease (AD) and the regulation of its production is an important therapeutic strategy. It was hypothesized in the present study that Nogo‑A may be involved in AD and may regulate the generation of Aβ. Nogo‑A is known to act as a major inhibitor of neuron regeneration in the adult central nervous system. A recent study indicated that Nogo‑A is associated with AD; however, the underlying effect and molecular mechanisms remain largely elusive. In the present study, the potential effects of Nogo‑A on AD were investigated. ELISA was used to detect the levels of Aβ, enzymatic activity detection kits were used to determine the activity of secretase enzymes in amyloid precursor protein (APP) metabolism, and western blot analysis was used to detect the expression levels of proteins associated with the APP processing and Nogo‑A/Nogo‑66 receptor (NgR) signaling pathways. The results revealed that Nogo‑66, the major inhibitory region of Nogo‑A, promoted neuronal Aβ secretion by increasing the activity of β‑secretase 1 via the NgR/Rho‑associated coiled‑coil containing kinases pathway in a dose‑dependent manner. The present data suggested that Nogo‑A may facilitate the onset and development of AD by promoting Aβ secretion, providing information on a potential novel target for AD therapy.
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