The Roles of Aβ in Alzheimer's Disease : In Light of the Latest Findings
The 'amyloid hypothesis', initially put forward in 1992, posits that amyloid β protein (Aβ) contributes to neurodegeneration through aberrant aggregation. In the process of this aberrant aggregation, Aβ forms oligomers, protofibrils, and mature fibrils, ultimately developing plaques. These mature fibrils and plaques were believed to be the culprits behind the neurotoxicity and neurodegeneration seen in Alzheimer's disease (AD). However, growing evidence in recent years has led to the 'Aβ oligomer hypothesis', which suggests that the intermediate forms of aggregates, such as oligomers and protofibrils, exhibit stronger neurotoxicity than the mature forms. Consequently, efforts have been made to develop anti-Aβ antibody drugs that specifically target these intermediate aggregates. Such interventions hold promise as disease-modifying treatments for AD.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:76 |
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| Enthalten in: |
Brain and nerve = Shinkei kenkyu no shinpo - 76(2024), 4 vom: 08. Apr., Seite 399-408 |
| Sprache: |
Japanisch |
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| Beteiligte Personen: |
Ono, Kenjiro [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 10.04.2024 Date Revised 10.04.2024 published: Print Citation Status MEDLINE |
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| doi: |
10.11477/mf.1416202619 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 520 | |a The 'amyloid hypothesis', initially put forward in 1992, posits that amyloid β protein (Aβ) contributes to neurodegeneration through aberrant aggregation. In the process of this aberrant aggregation, Aβ forms oligomers, protofibrils, and mature fibrils, ultimately developing plaques. These mature fibrils and plaques were believed to be the culprits behind the neurotoxicity and neurodegeneration seen in Alzheimer's disease (AD). However, growing evidence in recent years has led to the 'Aβ oligomer hypothesis', which suggests that the intermediate forms of aggregates, such as oligomers and protofibrils, exhibit stronger neurotoxicity than the mature forms. Consequently, efforts have been made to develop anti-Aβ antibody drugs that specifically target these intermediate aggregates. Such interventions hold promise as disease-modifying treatments for AD | ||
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| 700 | 1 | |a Nakamura, Yosuke |e verfasserin |4 aut | |
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