Amyloid β1 42 aβ1 42

Amyloid-β1–42 (Aβ1–42) was obtained from Sigma-Aldrich (St. Louis, MO, USA). Before injection, the Aβ1–42 peptide was dissolved in a physiological saline solution at a concentration of 5 mg/ml and incubated at 37°C for 72 h to induce aggregation. Human full length BDNF (ab9794), NGF (ab138794) and NT-3 (ab138798) proteins and their corresponding rabbit polyclonal antibodies (ab75040, ab6198 and ab65804) were purchased from Abcam (Cambridge, UK). Rabbit monoclonal antibodies against phospho-ERK (#4370), total ERK (#4695), phospho-JNK (#4668), total JNK (#9258), phospho-p38 (#4511), total p38 (#9212) and GAPDH (#5174) were from Cell Signaling Technology (Beverly, MA, USA). Ceramide C6, an ERK activator, was obtained from Santa Cruz Technology (Santa Cruz, CA, USA). The ERK inhibitor PD98059 was from Sigma-Aldrich (St. Louis, MO, USA).

Curcumin and amyloid-β1–42 (Aβ1–42) were obtained from Sigma-Aldrich (St. Louis, MO, USA). Prior to injection, the Aβ1–42 peptide was dissolved in a physiological saline solution at a concentration of 5 mg/ml and incubated at 37°C for 72 h to induce aggregation. Human full-length BDNF proteins and rabbit monoclonal antibodies against phospho-GSK 3β (Ser 9) and total GSK 3β were purchased from Abcam (Cambridge, UK). Rabbit polyclonal antibodies against BDNF, phospho-ERK (Thr202/Tyr204), total ERK, phospho-JNK (Thr183/Tyr185), total JNK, phospho-p38 (Thr180/Tyr182), and total p38 and GAPDH were obtained from Cell Signaling Technology (Beverly, MA, USA). The GSK-3 modulators, wortmannin, and ERK inhibitor PD98059 were obtained from Sigma-Aldrich (St. Louis, MO, USA). We used commercial lentiviral-BDNF shRNA particles and control non-targeting shRNA lentiviral particles, both of which were obtained from Santa Cruz (Santa Cruz Technology, CA, USA).