The DOI matches its Crossref record; 351 of the 355 references it cites were found in a registry or an index.
Amyloid β-interacting partners in Alzheimer's disease: From accomplices to possible therapeutic targets
Abstract
Alzheimer's disease (AD) is one of the most devastating neurodegenerative diseases in modern society because of insurmountable difficulties in early diagnosis and lack of therapeutic treatments. AD pathogenesis is tightly linked to the abnormal accumulation and aggregation of amyloid β (Aβ), seemingly the main causative factor of AD; however, intensive research on Aβ has not yet explained the complexity of AD pathogenesis. Consequently, the role of other supportive partners of Aβ have been elucidated and evaluated in the etiology of AD, and their potential molecular mechanisms have emerged as possible therapeutic targets. In this review, we compile information regarding Aβ-interacting partners in normal conditions and AD pathology, and analyze their etiological roles in diverse areas. Furthermore, we integrate this information into suggestions for probable clinical applications for AD diagnosis and therapeutics. We include Aβ-interacting partners localized to the cell surface and intracellular and extracellular compartments of different cell types ranging from the central nervous system to peripheral regions. Additionally, we expand the range of Aβ-interacting partners by including not only proteins, but also inorganic substances like metals, expecting that one of these partners may yield a critical breakthrough in the field of AD diagnostics and therapeutic drug development.
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“Overexpression of LRP minireceptor increased toxic amyloid β levels and caused the deficits in learning and memory, whereas LDLR overexpression decreased amyloid β accumulation [18].”
From Apolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease (2017) · cites this paper as [18]
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2 retracted
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RetractedThe precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor
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Toll-like receptors and innate immunity
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Decreased Clearance of CNS β-Amyloid in Alzheimer’s Disease
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Extracellular protein components of amyloid plaques and their roles in Alzheimer’s disease pathology
Rahman, M. M., & Lendel, C. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00465-0 · Cited by 260
Peripheral inflammatory biomarkers in Alzheimer’s disease: a brief review
Park, J., Han, S.-H., & Mook‐Jung, I. (2020) · BMB Reports · doi:10.5483/bmbrep.2020.53.1.309 · Cited by 206
Self-citationApolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease
Liao, F., Yoon, H., & Kim, J. (2017) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000383 · Cited by 191
Park, J., Han, S.-H., Yi, D., Byun, M. S., Lee, J. H., Jang, S. S., Ko, K., Jeon, S. Y., Lee, Y., Kim, Y. K., et al. (2018) · Brain · doi:10.1093/brain/awy347 · Cited by 181
Self-citationHussien, H. M., Abd-Elmegied, A., Ghareeb, D. A., Hafez, H. S., Ahmed, H. E. A., & Moneam, N. M. A. E. (2017) · Food and Chemical Toxicology · doi:10.1016/j.fct.2017.11.025 · Cited by 176
Metadata
- Authors
- Han, S.-H., Park, J.-C., & Mook-Jung, I.
- Affiliations
- Seoul National University (KR)
- ORCID
- Park, Jong-Chan
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2016-02
- Volume
- 137
- Pages
- 17-38
- ISSN
- 0301-0082 (ISSN-L)
- OpenAlex
- W2207689373
- Cited by
- 67
- References
- 355
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 4 · 2023: 4 · 2022: 4 · 2021: 11 · 2020: 5 · 2019: 10 · 2018: 9 · 2017: 12 · 2016: 4
- FWCI
- 1.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Progress in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- NRF (2015R1A2A1A05001794, 2014M3C7A1046047, 2015M3C7A1028790, 2015R1C1A2A01053545)
- MRC (2012R1A5A2A44671346)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta, protein-protein interaction, amyloid fibril formation, AD pathogenesis, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Blood Proteins, Brain, Humans, Metals, Prions, Receptors, Cell Surface, Amyloid beta-Peptides, LDL-Receptor Related Proteins, Apolipoprotein E4
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