The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Reduction of amyloid load and cerebral damage in transgenic mouse model of Alzheimer's disease by treatment with a β‐sheet breaker peptide
Abstract
Genetic, neuropathological, and biochemical studies have provided strong evidence for a central role of amyloid in the pathogenesis of Alzheimer's disease (AD). We have proposed previously that peptides designed as β‐sheet breakers may be useful in preventing the formation of amyloid plaques. In this study, we describe a modified β‐sheet breaker peptide with improved pharmacological properties, a high rate of penetration across the blood‐brain barrier, and the ability to induce a dramatic reduction in amyloid deposition in two different transgenic AD models. In addition, we report for the first time a significant increase in neuronal survival and a decrease in brain inflammation associated with the reduction of amyloid plaques. These results demonstrate that the process of amyloid deposition is one of the causes of neurodegeneration in AD. Moreover, our findings indicate that β‐sheet breaker peptides provide a valuable tool for evaluating further the importance of amyloid in the etiology of AD and suggest that these peptides or some of their derivatives might be good candidates for AD treatment.
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Cites
Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse
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Arrest of -Amyloid Fibril Formation by a Pentapeptide Ligand
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Self-citationAqueous Dissolution of Alzheimer's Disease Aβ Amyloid Deposits by Biometal Depletion
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ALZHEIMER'S DISEASE: Genetic Studies and Transgenic Models
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Cited by
Blennow, K., de Leon, M. J., & Zetterberg, H. (2006) · The Lancet · doi:10.1016/s0140-6736(06)69113-7 · Cited by 3,134
Molecular Mechanisms of Amyloidosis
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Unfolding the role of protein misfolding in neurodegenerative diseases
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Self-citationTreatment of Alzheimer's disease; current status and new perspectives
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Agrawal, M., Saraf, S., Saraf, S., Antimisiaris, S. G., Chougule, M. B., Shoyele, S. A., & Alexander, A. (2018) · Journal of Controlled Release · doi:10.1016/j.jconrel.2018.05.011 · Cited by 630
Metadata
- Authors
- Permanne, B., Adessi, C., Saborio, G. P., Fraga, S., Frossard, M., Van Dorpe, J., Dewachter, I., Banks, W. A., Van Leuven, F., & Soto, C.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2002-04-10
- Volume
- 16
- Issue
- 8
- Pages
- 860-862
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2113467168
- Cited by
- 220
- References
- 9
- FWCI
- 8.45
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Reduction of amyloid load and cerebral damage in transgenic mouse model of Alzheimer's disease by treatment with a β‐sheet breaker peptide. https://app.cochat.ai/papers/10.1096/fj.01-0841fje
- The paper
- Permanne, B., Adessi, C., Saborio, G. P., Fraga, S., Frossard, M., Van Dorpe, J., Dewachter, I., Banks, W. A., Van Leuven, F., & Soto, C. (2002). Reduction of amyloid load and cerebral damage in transgenic mouse model of Alzheimer's disease by treatment with a β‐sheet breaker peptide. The FASEB Journal. https://doi.org/10.1096/fj.01-0841fje
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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