ReviewMolecular biology reports2025
Transthyretin as a therapeutic target: the future of disease-modifying therapies for Alzheimer's disease.
Review in Molecular biology reports, 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.
- Therapeutic Potential ofJournal of inflammation research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlzheimer's disease (AD) is the most common neurodegenerative disease for causing memory deficits and primarily characterized by extracellular deposition of amyloid-β (Aβ) plaques, intracellular neurofibrillary tangles (NFTs), and hyperphosphorylation of tau protein, all are pathological hallmarks for AD. Transthyretin (TTR) is a highly conserved homo-tetrameric protein, primarily synthesized in liver and choroid plexus, and most importantly involved in transport of T
objectivesThis review explores the dual role of TTR, with a greater emphasis on its neuroprotective action, particularly in AD.
methodsBased on the available literature, TTR's potential as a biomarker in the central nervous system (CNS), focusing its role in stabilizing Aβ aggregation and the senile plaque formation during neurodegeneration. Additionally, TTR's dual roles, in neurodegeneration and neuroprotection are studied, emphasizing its potential for improving AD diagnosis and treatment strategies.
resultsRecent research has revealed that TTR is gradually showcasing its promise in neuroprotection and neuronal viability in AD by binding with Aβ and mitigating its neurotoxic effects. Current preclinical and clinical studies also support that TTR is actively involved in maintaining the blood-brain barrier (BBB) integrity and maintain neurotransmitter balance, all of which offer significant therapeutic promise through TTR stabilizers, such as Tafamidis, Acoramidis, and Vutrisiran, highlighting their potential in AD treatment
conclusionThis review concludes that TTR plays bidirectional role and gaining interest as a potential biomarker, though several challenges must be addressed before it can be established a novel therapeutic target in AD management in the modern era of drug discovery.
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Identifiers
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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.