Background
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder mainly characterized by the abnormal accumulation of β-amyloid (Aβ) peptide. The oligomeric form of the Aβ peptide as being the critical initiator of neurotoxicity in the AD pathogenesis[4].
Specific Modeling Methods
Rat: Wistar male adult, weighing 240-260 g
Administration: 1 μg/μL Hippocampal injection single dose
Note
(1) β-Amyloid (1-42) needs to be processed into oligomers before use.
(2) β-Amyloid (1-42) was injected bilaterally into the hippocampus of rat brain in a volume of 1.0 μL over a period of 0.1 μL/min using 1 μL Hamilton syringe.
Modeling Indicators
Indicator changes: Decreased the gene expression level of α7-nAChR and increased the mRNA expression of NMDA receptor 2A, and -2B subunits.
Behavior: β-Amyloid (1-42) aggregates increased the retention time and altered the behavioral response in rats after 15 days of injection.
Correlated Product(s): β-Amyloid (1-42), (rat/mouse) TFA (HY-P1388A);
β-Amyloid (1-40) (rat) (HY-P1387);
β-Amyloid (1-40) TFA (HY-P0265A)
Opposite Product(s): /
