TY - JOUR
T1 - Nanomedicine against Aβ aggregation by β–sheet breaker peptide delivery
T2 - In vitro evidence
AU - Pederzoli, Francesca
AU - Ruozi, Barbara
AU - Duskey, Jason
AU - Hagmeyer, Simone
AU - Sauer, Ann Katrin
AU - Grabrucker, Stefanie
AU - Coelho, Romina
AU - Oddone, Natalia
AU - Ottonelli, Ilaria
AU - Daini, Eleonora
AU - Zoli, Michele
AU - Vandelli, Maria Angela
AU - Tosi, Giovanni
AU - Grabrucker, Andreas M.
N1 - Publisher Copyright:
© 2019 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2019/11
Y1 - 2019/11
N2 - The accumulation of amyloid β (Aβ) triggers a cascade of toxic events in Alzheimer’s disease (AD). The KLVFF peptide can interfere with Aβ aggregation. However, the peptide suffers from poor bioavailability and the inability to cross the blood–brain barrier. In this work, we study the possibility of adopting nanomedicine to overcome KLVFF limits in biodistribution. We produced new engineered polymeric nanoparticles (NPs), and we evaluated the cellular toxicity of these NPs and validated that KVLFF peptides released by NPs show the same promising effects on AD pathology. Our results revealed the successful generation of KVLFF loaded NPs that, without significant effects on cell heath, are even more potent in reversing Aβ-induced pathologies compared to the free peptide. Therefore, NPs will significantly advance KVLFF treatment as a therapeutic option for AD.
AB - The accumulation of amyloid β (Aβ) triggers a cascade of toxic events in Alzheimer’s disease (AD). The KLVFF peptide can interfere with Aβ aggregation. However, the peptide suffers from poor bioavailability and the inability to cross the blood–brain barrier. In this work, we study the possibility of adopting nanomedicine to overcome KLVFF limits in biodistribution. We produced new engineered polymeric nanoparticles (NPs), and we evaluated the cellular toxicity of these NPs and validated that KVLFF peptides released by NPs show the same promising effects on AD pathology. Our results revealed the successful generation of KVLFF loaded NPs that, without significant effects on cell heath, are even more potent in reversing Aβ-induced pathologies compared to the free peptide. Therefore, NPs will significantly advance KVLFF treatment as a therapeutic option for AD.
KW - Alzheimer disease (AD)
KW - Amyloid β
KW - Aβ
KW - Blood-brain barrier (BBB)
KW - KLVFF peptide
KW - Polymeric nanoparticles (NPs)
UR - http://www.scopus.com/inward/record.url?scp=85075892911&partnerID=8YFLogxK
U2 - 10.3390/pharmaceutics11110572
DO - 10.3390/pharmaceutics11110572
M3 - Article
AN - SCOPUS:85075892911
SN - 1999-4923
VL - 11
JO - Pharmaceutics
JF - Pharmaceutics
IS - 11
M1 - 572
ER -