1.We characterized the pharmacokinetics of tafamidis, a novel drug to treat transthyretin-related amyloidosis, in rats after intravenous and oral administration at doses of 0.3-3 mg/kg.
10<sup>6</sup> MSC were injected into APP/PS1 mice via the tail vein and histological analysis was performed for microglia and amyloid (pE3-Aβ) plaque numbers, glial distribution and pE3-Aβ plaque size.
123I-labeled human SAP was injected intravenously into 20 controls and 189 consecutive patients with histologically proven amyloidosis: of AA type in 60 cases, AL type in 80, hereditary ATTR type in 27, and localized amyloidosis in 22 cases.
8-month-old female wild type (WT) and APP/PS1 mice were also administered daily NaCl or LiCl for 21 days, which was followed by cognitive assessment by novel object recognition and water maze, and measurement of soluble Aβ<sub>42</sub>, plaque-associated Aβ<sub>42</sub>, and brain efflux of <sup>125</sup>I-Aβ<sub>42</sub>.
Amyloid-beta (Abeta) the primary component of the senile plaques found in Alzheimer's disease (AD) is generated by the rate-limiting cleavage of amyloid precursor protein (APP) by beta-secretase followed by gamma-secretase cleavage.
Amyloid is mainly composed by amyloid-beta (A(beta)) peptides, which are derive from processing of the beta-amyloid precursor protein (APP), better named amyloid-beta precursor protein (A(beta)PP), by secretases.