The DOI matches its Crossref record; 122 of the 122 references it cites were found in a registry or an index.
Mechanisms of Amyloid-β Peptide Clearance: Potential Therapeutic Targets for Alzheimer's Disease
Open accessAbstract
Amyloid-β peptide (Aβ) is still best known as a molecule to cause Alzheimer's disease (AD) through accumulation and deposition within the frontal cortex and hippocampus in the brain. Thus, strategies on developing AD drugs have been focused on the reduc-tion of Aβ in the brain. Since accumulation of Aβ depends on the rate of its synthesis and clearance, the metabolic pathway of Aβ in the brain and the whole body should be carefully explored for AD research. Although the synthetic pathway of Aβ is equally important, we summarize primarily the clearance pathway in this paper because the former has been extensively reviewed in previous studies. The clearance of Aβ from the brain is accomplished by several mechanisms which include non-enzymatic and enzymatic pathways. Nonenzymatic pathway includes interstitial fluid drainage, uptake by microglial phagocytosis, and transport across the blood vessel walls into the circulation. Multiple Aβ-degrading enzymes (ADE) implicated in the clearance process have been identified, which include neprilysin, insulin-degrading enzyme, matrix metalloproteinase-9, glutamate carboxypeptidase II and others. A series of studies on Aβ clearance mechanism provide new insight into the pathogenesis of AD at the molecular level and suggest a new target for the development of novel therapeutics.
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In the citing paper
“forming a protective barrier to protect brain tissue from the neurotoxicity of Aβ plaques”
From Acoustofluidic assembly of 3D neurospheroids to model Alzheimer's disease (2020) · cites this paper as [47]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“promotes the clearance of Aβ aggregates.47, 48”
From Acoustofluidic assembly of 3D neurospheroids to model Alzheimer's disease (2020) · cites this paper as [47]
In the citing paper
“The Aβ clearance may occur through the transport into the cerebrospinal fluid, the blood across the blood-brain barrier (BBB), and the removal by brain-resident macrophages (Yoon and Jo, 2012).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Yoon and Jo, 2012
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1 retracted
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Cited by
Sorted by citations
Clearance systems in the brain—implications for Alzheimer disease
Tarasoff-Conway, J. M., Carare, R. O., Osorio, R. S., Glodzik, L., Butler, T., Fieremans, E., Axel, L., Rusinek, H., Nicholson, C., Zlokovic, B. V., et al. (2015) · Nature Reviews Neurology · doi:10.1038/nrneurol.2015.119 · Cited by 1,678
The Role of Amyloid-β Oligomers in Toxicity, Propagation, and Immunotherapy
Sengupta, U., Nilson, A. N., & Kayed, R. (2016) · EBioMedicine · doi:10.1016/j.ebiom.2016.03.035 · Cited by 740
“Therefore, any imbalance in the dynamic equilibrium maintained by these three pathways would result in the accumulation of Aβ (Yoon and Jo, 2012; Mucke, 2009).”
BackgroundMechanisms of Aβ Clearance and Degradation by Glial Cells
Ries, M., & Sastre, M. (2016) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2016.00160 · Cited by 527
“A great number of reviews have examined the main mechanisms of Aβ clearance and degradation (Bates et al., 2009; Saido and Leissring, 2012; Yoon and Jo, 2012; Tarasoff-Conway et al., 2015).”
BackgroundZhong, L., Xu, Y., Zhuo, R., Wang, T., Wang, K., Huang, R., Wang, D., Gao, Y., Zhu, Y., Sheng, X., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-09118-9 · Cited by 371
The Translational Significance of the Neurovascular Unit
McConnell, H. L., Kersch, C. N., Woltjer, R. L., & Neuwelt, E. A. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.r116.760215 · Cited by 314
Metadata
- Authors
- Yoon, S.-S., & AhnJo, S.-M.
- Affiliations
- Dankook University (KR)
- ORCID
- Yoon, Sang-Sun
- Venue
- Biomolecules and Therapeutics
- Published
- 2012-05-31
- Volume
- 20
- Issue
- 3
- Pages
- 245-255
- ISSN
- 1976-9148 (ISSN-L)
- PMC
- PMC3794520
- OpenAlex
- W2008487250
- Cited by
- 205
- References
- 122
- Citations by year
- 2026: 15 · 2025: 27 · 2024: 27 · 2023: 23 · 2022: 14 · 2021: 26 · 2020: 18 · 2019: 15 · 2018: 11 · 2017: 9 · 2016: 6 · 2015: 9 · 2014: 1 · 2013: 3 · 2012: 1
- FWCI
- 0.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biomolecules & Therapeutics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- National Research Foundation
- National Research Foundation of Korea (2011-0016127)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- amyloid-beta, Alzheimer's disease, amyloid-beta clearance, neprilysin, insulin-degrading enzyme, MMP-9, prostate-specific membrane antigen, microglial phagocytosis, interstitial fluid drainage, blood-brain barrier, therapeutic target
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