ArticleScientific reports2013
Cessation of neoangiogenesis in Alzheimer's disease follows amyloid-beta immunization.
Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 33 citations in OpenAlex.
- Dysfunction of the neurovascular unit as a temporal driver in Alzheimer's pathogenesis.Translational neurodegeneration · 2026Review
- The Cerebrovascular Side of Plasticity: Microvascular Architecture across Health and Neurodegenerative and Vascular Diseases.Brain sciences · 2024Review
- Conclusive demonstration of iatrogenic Alzheimer's disease transmission in a model of stem cell transplantation.Stem cell reports · 2024Article
- Endothelial Senescence and Its Impact on Angiogenesis in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Prostacyclin Promotes Degenerative Pathology in a Model of Alzheimer's Disease.Frontiers in cellular neuroscience · 2022Article
- PKCε Activation Restores Loss of PKCε, Manganese Superoxide Dismutase, Vascular Endothelial Growth Factor, and Microvessels in Aged and Alzheimer's Disease Hippocampus.Frontiers in aging neuroscience · 2022Article
- A Nanomule Peptide Carrier Delivers siRNA Across the Intact Blood-Brain Barrier to Attenuate Ischemic Stroke.Frontiers in molecular biosciences · 2021Article
- The physiological roles of tau and Aβ: implications for Alzheimer's disease pathology and therapeutics.Acta neuropathologica · 2020Review
- Microvascular Alterations in Alzheimer's Disease.Frontiers in cellular neuroscience · 2020Review
- Neurovascular Unit Dysfunction and Neurodegenerative Disorders.Frontiers in neuroscience · 2020Review
- Vascular Dysfunction in Alzheimer's Disease: A Prelude to the Pathological Process or a Consequence of It?Journal of clinical medicine · 2019Review
- Dissecting the Contribution of Vascular Alterations and Aging to Alzheimer's Disease.Molecular neurobiology · 2016Review
- Involvement of matrix metalloproteinase-9 in amyloid-β 1-42-induced shedding of the pericyte proteoglycan NG2.Journal of neuropathology and experimental neurology · 2014Article
- Iron deposits in the chronically inflamed central nervous system and contributes to neurodegeneration.Cellular and molecular life sciences : CMLS · 2014Review
- Immunotherapy for the treatment of Alzheimer's disease: amyloid-β or tau, which is the right target?ImmunoTargets and therapy · 2014Review
- Adjusting the compass: new insights into the role of angiogenesis in Alzheimer's disease.Alzheimer's research & therapy · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Pathogenic neoangiogenesis in Alzheimer's disease (AD) is due to amyloid-beta (Aβ) and results in blood-brain barrier (BBB) leakiness in AD. It likely occurs as a compensatory response to impaired cerebral blood flow and provides a strong link between brain vascularity and AD. Aβ immunotherapy is an experimental treatment for AD; however, unexpected negative vascular side effects seen in early human clinical trials demonstrate that our knowledge of Aβ and AD pathogenesis is incomplete. We demonstrate that immunization with Aβ peptides neutralizes the amyloid trigger leading to neoangiogenesis and reverses hypervascularity in Tg2576 AD mice. This process resolves plaque burden suggesting that neoangiogenesis is a key mechanism underlying plaque formation. A meta-analysis demonstrated that hypervascular reversion in vaccinated Alzheimer's patients. This appears to be the first example of vascular reversion following any therapeutic intervention and supports the conclusion that modulation of neoangiogenesis may repair damage in the AD brain.
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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.