SynthesisCNS neuroscience & therapeutics2025
Osteopontin in Alzheimer's Disease: A Double-Edged Sword in Neurodegeneration and Neuroprotection-A Systematic Review.
Synthesis 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 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Context-dependent roles of osteopontin in aging-related neurological disorders.The Journal of international medical research · 2026Review
- Neuron-derived SPP1 instructs microglia to limit degeneration.Science advances · 2026Article
- Development and Validation of a Predictive Model for Mild Cognitive Impairment in Older Adults with Multimorbidity.Clinical interventions in aging · 2026Article
- SPP1 (osteopontin): a key regulator orchestrating cancer progression and non-cancerous pathologies - therapeutic opportunities and future directions.Frontiers in cell and developmental biology · 2026Review
- Associations between cerebrospinal fluid biomarkers related to endothelial dysfunction and Alzheimer's disease.Frontiers in aging neuroscience · 2026Article
- Unraveling the Bone-Brain Communication Network.Biology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOsteopontin (OPN) has emerged as a pivotal molecule in Alzheimer's disease (AD), with studies indicating its potential to act as both a neuroprotective agent and a contributor to neurodegeneration. This systematic review aims to elucidate the roles of OPN in AD pathogenesis through inflammatory pathways.
methodsWe conducted a comprehensive analysis of current literature on OPN's involvement in AD, focusing on its signaling pathways, cellular interactions, and regulatory mechanisms. We searched PubMed, EMBASE, and Scopus databases by the keyword of Alzheimer's Disease and Osteopontin. Our date search was in 1990 until July 1, 2024 with no language limitation.
resultsIn a review of 758 studies, a total of 15 reports met the eligibility criteria and were included. Among the findings, four studies provided evidence supporting the protective mechanism of OPN within the context of AD. Eleven studies explain the inflammatory role of OPN. OPN has been shown to play a role in synaptic pruning, microglial activation, and the inflammatory processes associated with AD. Additionally, OPN is implicated in facilitating cellular communication and serves as a chemotactic molecule. It is suggested that the protective effects of OPN are predominantly mediated by the c fragment of the protein and are most prominent in the early stages of AD progression.
conclusionOPN in AD has dual effects-protecting neurons and contributing to their degeneration. Future research should enhance its protective mechanisms, target specific signaling pathways, and develop therapies to slow AD progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.