SynthesisThe Journal of physiology2026
The causative role of amyloidosis in the cardiac complications of Alzheimer's disease: a comprehensive systematic review.
Synthesis in The Journal of physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- AmyloGram reveals amyloidogenic potential in stroke thrombus proteomes.The Biochemical journal · 2025Article
- The heart-brain axis: unraveling the interconnections between cardiovascular and Alzheimer's diseases.Frontiers in cardiovascular medicine · 2025Review
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
Abstract
Alzheimer's disease (AD), the leading cause of dementia, is characterised by cerebral amyloid-beta (Aβ) and tau deposition, impairing cognition. While cardiovascular diseases exacerbate AD, the reverse association is underappreciated. This systematic review examined clinical and experimental studies that explored the cardiogenic dementia hypothesis and mechanisms by which amyloidosis in AD contributes to cardiovascular complications. A review of PubMed, Ovid Embase/Medline, and CINAHL conducted in August 2024 identified 252 studies meeting the selection criteria. Evidence links cerebral hypoperfusion from cardiac arrest, heart failure, or orthostatic hypotension to AD pathology, while atherosclerosis and hypertension drive neurodegeneration and cerebral amyloidosis. Vascular scoring tools, such as the Framingham Risk Score, may predict an individual's risk of cognitive impairment. Cardiac amyloidosis correlated with ECG abnormalities, aortic valve calcification, cardiomyopathy and atrial fibrillation. Aβ peptides and AD-related genes exacerbate cardiac fibrosis, negative inotropy and heart rate changes, reduce nitric oxide-mediated vasodilatation, and increase oxidative stress. Preclinical studies revealed that β-secretase impacts cardiac repolarisation by interfering with delayed rectifier current, although clinical evidence for arrhythmogenesis remains conflicting. AD-related autonomic dysregulation, particularly parasympathetic dysfunction, predisposes to arrhythmias. Additionally, hypercortisolaemia observed in AD has been associated with increased arterial stiffness. Diminished melatonin levels in AD were also linked to endothelial and mitochondrial dysfunction. This review enhances our understanding of how cerebral and cardiac amyloidosis, autonomic dysfunction, and endocrinopathy contribute to cardiac complications in AD, paving the way for research into targeted therapies.
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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.