ReviewAIMS neuroscience2025
A review on recent advances in Alzheimer's disease: The role of synaptic plasticity.
Review in AIMS neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Impaired TGFβ Signaling in Plaque-Associated Microglia.Biomolecules · 2026Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's Disease (AD) remains a significant global health challenge, characterized by progressive neurodegeneration and a decline in cognitive abilities such as memory and learning. Despite being the main cause of dementia worldwide, the precise mechanisms that underlie neuronal dysfunction and synaptic plasticity impairment in AD remain elusive. However, while genetic mutations, dietary factors, and immune dysregulation are implicated in AD pathogenesis, the current therapeutic approaches are largely centered around acetylcholinesterase inhibitors (AChEIs). Nevertheless, this cholinergic hypothesis of AD is no longer satisfactory in describing this disease and has demonstrated a limited efficacy. Hence, new treatment approaches should be developed, and that requires us to view AD from a new perspective. Herein, in our review, we present the latest studies that discussed possible AD pathologies and pharmacotherapies. Additionally, we highlight that the emerging treatments that precisely targets brain regions associated with enhancing neuroplasticity have delivered promising results and seem to be more effective than older treatments. Finally, by viewing AD as a complex interplay of various factors that ultimately cause synaptic dysfunction and cognitive decline, we can develop more effective therapeutic interventions and ultimately alleviate the significant burden of this debilitating disease for both patients and their families.
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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 Socratic graph.