Amyloid-β Contributes to Blood–Brain Barrier Leakage in Transgenic Human Amyloid Precursor Protein Mice and in Humans With Cerebral Amyloid Angiopathy | Zendy

Anika M. S. Hartz | Zendy; Björn Bauer | Zendy; Emma L. B. Soldner | Zendy; Andrea Wolf | Zendy; Sandra Boy | Zendy; Roland Backhaus | Zendy; Ivan Mihaljević | Zendy; Ulrich Bogdahn | Zendy; Hans H. Klünemann | Zendy; Gerhard Schuierer | Zendy; Felix Schlachetzki | Zendy

Open Access

Amyloid-β Contributes to Blood–Brain Barrier Leakage in Transgenic Human Amyloid Precursor Protein Mice and in Humans With Cerebral Amyloid Angiopathy

Author(s) -

Anika M. S. Hartz,

Björn Bauer,

Emma L. B. Soldner,

Andrea Wolf,

Sandra Boy,

Roland Backhaus,

Ivan Mihaljević,

Ulrich Bogdahn,

Hans H. Klünemann,

Gerhard Schuierer,

Felix Schlachetzki

Publication year - 2011

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.111.627562

Subject(s) - cerebral amyloid angiopathy , blood–brain barrier , pathology , medicine , tight junction , genetically modified mouse , amyloid (mycology) , transgene , dementia , endocrinology , biology , microbiology and biotechnology , central nervous system , biochemistry , disease , gene

Cerebral amyloid angiopathy (CAA) is a degenerative disorder characterized by amyloid-β (Aβ) deposition in the blood-brain barrier (BBB). CAA contributes to injuries of the neurovasculature including lobar hemorrhages, cortical microbleeds, ischemia, and superficial hemosiderosis. We postulate that CAA pathology is partially due to Aβ compromising the BBB.

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