Rosiglitazone rescues memory impairment in Alzheimer's transgenic mice: mechanisms involving a reduced amyloid and tau pathology
L Escribano, AM Simón, E Gimeno… - …, 2010 - nature.com
Clinical studies suggest that agonists at peroxisome proliferator-activated receptor gamma
(PPARγ) may exert beneficial effects in patients with mild-to-moderate Alzheimer's disease
(AD), but the mechanism for the potential therapeutic interest of this class of drugs has not
yet been elucidated. Here, in mice overexpressing mutant human amyloid precursor protein,
we found that chronic treatment with rosiglitazone, a high-affinity agonist at PPARγ,
facilitated β-amyloid peptide (Aβ) clearance. Rosiglitazone not only reduced Aβ burden in …
(PPARγ) may exert beneficial effects in patients with mild-to-moderate Alzheimer's disease
(AD), but the mechanism for the potential therapeutic interest of this class of drugs has not
yet been elucidated. Here, in mice overexpressing mutant human amyloid precursor protein,
we found that chronic treatment with rosiglitazone, a high-affinity agonist at PPARγ,
facilitated β-amyloid peptide (Aβ) clearance. Rosiglitazone not only reduced Aβ burden in …
Rosiglitazone Rescues Memory Impairment in Alzheimer's Transgenic Mice: Mechanisms Involving a Reduced Amyloid and Tau Pathology
D Frechilla, LA Perez-Mediavilla, A Ricobaraza… - 2010 - dadun.unav.edu
Clinical studies suggest that agonists at peroxisome proliferator-activated receptor gamma
(PPARγ) may exert beneficial effects in patients with mild-to-moderate Alzheimer's disease
(AD), but the mechanism for the potential therapeutic interest of this class of drugs has not
yet been elucidated. Here, in mice overexpressing mutant human amyloid precursor protein,
we found that chronic treatment with rosiglitazone, a high-affinity agonist at PPARγ,
facilitated β-amyloid peptide (Aβ) clearance. Rosiglitazone not only reduced Aβ burden in …
(PPARγ) may exert beneficial effects in patients with mild-to-moderate Alzheimer's disease
(AD), but the mechanism for the potential therapeutic interest of this class of drugs has not
yet been elucidated. Here, in mice overexpressing mutant human amyloid precursor protein,
we found that chronic treatment with rosiglitazone, a high-affinity agonist at PPARγ,
facilitated β-amyloid peptide (Aβ) clearance. Rosiglitazone not only reduced Aβ burden in …
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