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Amyloid-β Peptides, Alzheimer's Disease and the Blood-brain Barrier
Abstract
Ever since amyloid-β (Aβ) peptides were first identified in cerebral plaques in patients with Alzheimer's disease (AD), much research work has focused on the complex mechanisms through which these peptides are synthesized, transported and degraded. Although new information emerges on a regular basis, we consider that the importance of the blood-brain barrier (BBB) in the pathogenesis of AD has been underestimated. In fact, there are a number of obstacles that make it difficult to convince specialists in AD that the BBB indeed plays a key role in this disease: these include the complex physiology of the BBB and the technical difficulty of studying the barrier in vivo and reproducing its main properties in vitro. With these considerations in mind, the present review sets out summarize our current knowledge about the physiology of the BBB and describe recent research findings on the barrier's role in Aβ peptide proteostasis and thus in the mechanism of AD.
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Dysregulation of brain cholesterol metabolism and Aβ peptide transport across the BBB are thought to have a key role in Alzheimer's disease.
“Dysregulation of brain cholesterol metabolism and A peptide transport across the BBB are thought to have a key role in the development of AD [25,47].”
ABCB1 and probably ABCC1 restrict Aβ re-entry into the brain.
“whereas ABCB1 and probably ABCC1 restrict A re-entry into the brain [25,37,38].”
The levels of ApoE and HDL (or HDL-like particles) are important parameters for the cholesterol shuttle between neurons and astrocytes and for the BBB-mediated clearance of Aβ peptides.
“The levels of ApoE and HDL (or HDL-like particles) are important parameters for the cholesterol shuttle between neurons and astrocytes and for the BBBmediated clearance of A peptides [9,25,47].”
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Targeting and Crossing the Blood-Brain Barrier with Extracellular Vesicles
Saint-Pol, J., Gosselet, F., Duban-Deweer, S., Pottiez, G., & Karamanos, Y. (2020) · Cells · doi:10.3390/cells9040851 · Cited by 503
Self-citationFahimi, A., Baktir, M. A., Moghadam, S., Mojabi, F. S., Sumanth, K., McNerney, M. W., Ponnusamy, R., & Salehi, A. (2017) · Brain Structure and Function · doi:10.1007/s00429-016-1308-8 · Cited by 94
Merino-Zamorano, C., Fernández-de Retana, S., Montañola, A., Batlle, A., Saint-Pol, J., Mysiorek, C., Gosselet, F., Montaner, J., & Hernández-Guillamon, M. (2016) · Journal of Alzheimer's Disease · doi:10.3233/jad-150976 · Cited by 63
Self-citationA New Hypothesis for Alzheimer’s Disease: The Lipid Invasion Model
Rudge, J. D. (2022) · Journal of Alzheimer's Disease Reports · doi:10.3233/adr-210299 · Cited by 58
Kuntz, M., Candela, P., Saint-Pol, J., Lamartinière, Y., Boucau, M.-C., Sevin, E., Fenart, L., & Gosselet, F. (2015) · Journal of Alzheimer's Disease · doi:10.3233/jad-150469 · Cited by 55
Self-citationMatsumoto, K., Chiba, Y., Fujihara, R., Kubo, H., Sakamoto, H., & Ueno, M. (2015) · Histochemistry and Cell Biology · doi:10.1007/s00418-015-1366-7 · Cited by 46
Metadata
- Authors
- Gosselet, F., Saint-Pol, J., Candela, P., & Fenart, L.
- Venue
- Current Alzheimer Research
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2013-12-31
- Volume
- 10
- Issue
- 10
- Pages
- 1015-1033
- ISSN
- 1567-2050
- Cited by
- 68
- References
- 0
- Language
- en
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