Open AccessS t. J ohn's W ort Reduces Beta‐Amyloid Accumulation in a Double Transgenic A lzheimer's Disease Mouse Model—Role of P ‐Glycoprotein
Author(s) -
Brenn Anja,
Grube Markus,
Jedlitschky Gabriele,
Fischer Andrea,
Strohmeier Barbara,
Eiden Martin,
Keller Markus,
Groschup Martin H.,
Vogelgesang Silke
Publication year - 2014
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/bpa.12069
Subject(s) - hypericum perforatum , hyperforin , genetically modified mouse , amyloid precursor protein , p glycoprotein , pharmacology , transgene , glycoprotein , chemistry , amyloid (mycology) , medicine , microbiology and biotechnology , alzheimer's disease , biochemistry , biology , disease , gene , pathology , multiple drug resistance , antibiotics
The adenosine triphosphate‐binding cassette transport protein P ‐glycoprotein ( ABCB1 ) is involved in the export of beta‐amyloid from the brain into the blood, and there is evidence that age‐associated deficits in cerebral P ‐glycoprotein content may be involved in A lzheimer's disease pathogenesis. P ‐glycoprotein function and expression can be pharmacologically induced by a variety of compounds including extracts of H ypericum perforatum ( S t. J ohn's W ort). To clarify the effect of S t. J ohn's W ort on the accumulation of beta‐amyloid and P ‐glycoprotein expression in the brain, S t. J ohn's W ort extract (final hyperforin concentration 5%) was fed to 30‐day‐old male C57BL/6J ‐ APP /PS1 +/− mice over a period of 60 or 120 days, respectively. Age‐matched male C57BL/6J ‐ APP / PS1 +/− mice receiving a S t. J ohn's W ort‐free diet served as controls. Mice receiving S t. J ohn's W ort extract showed (i) significant reductions of parenchymal beta‐amyloid 1–40 and 1–42 accumulation; and (ii) moderate, but statistically significant increases in cerebrovascular P ‐glycoprotein expression. Thus, the induction of cerebrovascular P ‐glycoprotein may be a novel therapeutic strategy to protect the brain from beta‐amyloid accumulation, and thereby impede the progression of A lzheimer's disease.