ReviewFrontiers in aging neuroscience2014
New therapeutic approaches for Alzheimer's disease and cerebral amyloid angiopathy.
Review in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 71 citations in OpenAlex.
- Efficacy and Safety of Cilostazol in Mild Cognitive Impairment: A Randomized Clinical Trial.JAMA network open · 2023Trial
- AβInternational journal of molecular sciences · 2025Article
- Article
- Oxidative Stress in Health and Disease.Biomedicines · 2023Review
- New Perspectives of Taxifolin in Neurodegenerative Diseases.Current neuropharmacology · 2023Review
- Perivascular spaces and brain waste clearance systems: relevance for neurodegenerative and cerebrovascular pathology.Neuroradiology · 2021Review
- Circulating AQP4 Levels in Patients with Cerebral Amyloid Angiopathy-Associated Intracerebral Hemorrhage.Journal of clinical medicine · 2021Article
- Taxifolin: A Potential Therapeutic Agent for Cerebral Amyloid Angiopathy.Frontiers in pharmacology · 2021Review
- Azeliragon ameliorates Alzheimer's disease via the Janus tyrosine kinase and signal transducer and activator of transcription signaling pathway.Clinics (Sao Paulo, Brazil) · 2021Article
- Repositioning medication for cardiovascular and cerebrovascular disease to delay the onset and prevent progression of Alzheimer's disease.Archives of pharmacal research · 2020Review
- Low-Dose Phosphodiesterase III Inhibitor Reduces the Vascular Amyloid Burden in Amyloid-β Protein Precursor Transgenic Mice.International journal of molecular sciences · 2020Article
- Potential Therapeutic Approaches for Cerebral Amyloid Angiopathy and Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Potential Role of Venular Amyloid in Alzheimer's Disease Pathogenesis.International journal of molecular sciences · 2020Review
- Roles of vascular risk factors in the pathogenesis of dementia.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Review
- Drug Development for Central Nervous System Diseases Using In vitro Blood-brain Barrier Models and Drug Repositioning.Current pharmaceutical design · 2020Review
- Quantitative proteomic profiling of white matter in cases of cerebral amyloid angiopathy reveals upregulation of extracellular matrix proteins and clusterin.Free neuropathology · 2020Article
- Clearance of interstitial fluid (ISF) and CSF (CLIC) group-part of Vascular Professional Interest Area (PIA): Cerebrovascular disease and the failure of elimination of Amyloid-β from the brain and retina with age and Alzheimer's disease-Opportunities for Therapy.Alzheimer's & dementia (Amsterdam, Netherlands) · 2020Article
- Accumulation of Amyloid Beta (Aβ) Peptide on Blood Vessel Walls in the Damaged Brain after Transient Middle Cerebral Artery Occlusion.Biomolecules · 2019Article
- Platelet-generated amyloid beta peptides in Alzheimer's disease and glaucoma.Histology and histopathology · 2019Review
- PDE3 Inhibitors Repurposed as Treatments for Age-Related Cognitive Impairment.Molecular neurobiology · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence has shown a strong relationship between Alzheimer's disease (AD), cerebral amyloid angiopathy (CAA), and cerebrovascular disease. Cognitive impairment in AD patients can result from cortical microinfarcts associated with CAA, as well as the synaptic and neuronal disturbances caused by cerebral accumulations of β-amyloid (Aβ) and tau proteins. The pathophysiology of AD may lead to a toxic chain of events consisting of Aβ overproduction, impaired Aβ clearance, and brain ischemia. Insufficient removal of Aβ leads to development of CAA and plays a crucial role in sporadic AD cases, implicating promotion of Aβ clearance as an important therapeutic strategy. Aβ is mainly eliminated by three mechanisms: (1) enzymatic/glial degradation, (2) transcytotic delivery, and (3) perivascular drainage (3-"d" mechanisms). Enzymatic degradation may be facilitated by activation of Aβ-degrading enzymes such as neprilysin, angiotensin-converting enzyme, and insulin-degrading enzyme. Transcytotic delivery can be promoted by inhibition of the receptor for advanced glycation end products (RAGE), which mediates transcytotic influx of circulating Aβ into brain. Successful use of the RAGE inhibitor TTP488 in Phase II testing has led to a Phase III clinical trial for AD patients. The perivascular drainage system seems to be driven by motive force generated by cerebral arterial pulsations, suggesting that vasoactive drugs can facilitate Aβ clearance. One of the drugs promoting this system is cilostazol, a selective inhibitor of type 3 phosphodiesterase. The clearance of fluorescent soluble Aβ tracers was significantly enhanced in cilostazol-treated CAA model mice. Given that the balance between Aβ synthesis and clearance determines brain Aβ accumulation, and that Aβ is cleared by several pathways stated above, multi-drugs combination therapy could provide a mainstream cure for sporadic AD.
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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.