ReviewFrontiers in cellular neuroscience2015
Role of amyloid peptides in vascular dysfunction and platelet dysregulation in Alzheimer's disease.
Review in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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.
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Who cites it
51 citing papers in PubMed, 99 citations in OpenAlex.
- Effect of a Comprehensive Intervention on Plasma BDNF in Patients with Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2017Trial
- Unveiling the procoagulant state in Alzheimer's disease: A novel PET imaging strategy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Review
- Neurovascular dysfunction in the development and progression of neuroinflammatory diseases.Frontiers in cellular neuroscience · 2026Review
- Post-marketing safety of lecanemab: a real-world study based on FAERS database, multicenter cohort and network pharmacology.Frontiers in psychiatry · 2026Article
- Associations between platelet indices and cerebrospinal fluid biomarkers of Alzheimer's disease pathology in cognitively intact adults: the CABLE study.Alzheimer's research & therapy · 2025Article
- Role of Thrombosis in Neurodegenerative Diseases: An Intricate Mechanism of Neurovascular Complications.Molecular neurobiology · 2025Review
- Alterations in the Processing of Platelet APP (Amyloid Beta Precursor Protein) in Alzheimer Disease: The Possible Nexus.Neuropsychopharmacology reports · 2025Review
- Computational insights into the aggregation mechanism and amyloidogenic core of aortic amyloid medin polypeptide.Colloids and surfaces. B, Biointerfaces · 2024Article
- Demystifying the Role of Neuroinflammatory Mediators as Biomarkers for Diagnosis, Prognosis, and Treatment of Alzheimer's Disease: A Review.ACS pharmacology & translational science · 2024Review
- Differential neuropsychiatric associations of plasma biomarkers in older adults with major depression and subjective cognitive decline.Translational psychiatry · 2024Article
- Retinal peri-arteriolar versus peri-venular amyloidosis, hippocampal atrophy, and cognitive impairment: exploratory trial.Acta neuropathologica communications · 2024Article
- The Role of NRF2 in Cerebrovascular Protection: Implications for Vascular Cognitive Impairment and Dementia (VCID).International journal of molecular sciences · 2024Review
- Impact of white matter hyperintensities on structural connectivity and cognition in cognitively intact ADNI participants.Neurobiology of aging · 2024Article
- Peripheral blood amyloid-β involved in the pathogenesis of Alzheimer's disease via impacting on peripheral innate immune cells.Journal of neuroinflammation · 2024Review
- Advances in Alzheimer's Disease Biomarkers.Current Alzheimer research · 2024Review
- Cerebrovascular Dysfunction in Alzheimer's Disease and Transgenic Rodent Models.Journal of experimental neurology · 2024Article
- Amyloid beta accumulation in TgF344-AD rats is associated with reduced cerebral capillary endothelial Kir2.1 expression and neurovascular uncoupling.GeroScience · 2023Article
- Article
- Dimethyl Fumarate as the Peripheral Blood Inflammatory Mediators Inhibitor in Prevention of Streptozotocin-Induced Neuroinflammation in Aged Rats.Journal of inflammation research · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common neurodegenerative cause of dementia in the elderly. AD is accompanied by the accumulation of amyloid peptides in the brain parenchyma and in the cerebral vessels. The sporadic form of AD accounts for about 95% of all cases. It is characterized by a late onset, typically after the age of 65, with a complex and still poorly understood aetiology. Several observations point towards a central role of cerebrovascular dysfunction in the onset of sporadic AD (SAD). According to the "vascular hypothesis", AD may be initiated by vascular dysfunctions that precede and promote the neurodegenerative process. In accordance to this, AD patients show increased hemorrhagic or ischemic stroke risks. It is now clear that multiple bidirectional connections exist between AD and cerebrovascular disease, and in this new scenario, the effect of amyloid peptides on vascular cells and blood platelets appear to be central to AD. In this review, we analyze the effect of amyloid peptides on vascular function and platelet activation and its contribution to the cerebrovascular pathology associated with AD and the progression of this disease.
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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.