CASP3 and amyloidosis: Taken together, these data indicate that the neuroprotective potential of hiMG during chronic Aβ exposure is highly time-dependent: At 3w Aβ, added hiMG preserved neuronal function, prevented oxidative stress, and reduced Caspase- 3 cleavage, while at 5w Aβ, hiMG did not rescue neuronal function or reduce oxidative stress but hiMG did significantly reduce apoptosis and loss of cell nuclei, demonstrating limited neuroprotection by hiMG at late stages of amyloidosis.