• Modeling Mechanism：

  β-Amyloid (1-42) (Aβ₁₋₄₂) acts as a ligand for the p75 neurotrophic factor receptor (p75ᴺᵀᴿ) in oligomeric form. Upon binding, it activates the neuronal death signaling pathway: promoting the cleavage of p75ᴺᵀᴿ extracellular domain metalloproteinases to generate apoptotic C-terminal fragment (CTF); at the same time, it inhibits γ-secretase activity, preventing further degradation of CTF, leading to CTF accumulation, and ultimately causing the degeneration of basal forebrain cholinergic neurons and hippocampal neuronal death, mimicking the core pathological features of AD.

• Related Products：

  β-Amyloid (1-42), rat/mouse (TP1230)

• Modeling Method：

  Experimental Subject：

  Mice: C57BL/6 (wild-type), p75 knockout (KO); Embryonic day 16 (E16, in vitro neuronal culture), 8 weeks of age (in vivo modelling)

  Dosage and Administration Route：

  100 μg/mL Aβ₁₋₄₂, 0.5 μL, Stereotaxic injection into hippocampal CA1 region (coordinates: anterior bregma-2.0 mm, lateral-1.3 mm, depth-2.2 mm)

  Dosing Frequency and Duration Model：

  Single dose

• Validation：

  Neuronal degeneration: The number of choline acetyltransferase (ChAT)-positive neurons in the basal forebrain of wild-type mice was significantly reduced, while no significant changes were observed in p75ᴺᵀᴿ knockout mice; Histology: No obvious tissue damage was observed at the injection site in the CA1 region of the hippocampus, consistent with the characteristics of selective neuronal degeneration in Alzheimer's disease (AD).

*Precautions： Execution and testing 14 days later

*References：Sotthibundhu A,et,al. Beta-amyloid(1-42) induces neuronal death through the p75 neurotrophin receptor. J Neurosci. 2008 Apr 9;28(15):3941-6.