{'fraction_non_alphanumeric': 0.030562347188264057, 'fraction_numerical': 0.02689486552567237, 'mean_word_length': 4.978102189781022, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Estrogen protects neuronal cells from amyloid β-induced apoptotic cell death

Accumulating studies have shown that estrogen replacement therapy reduces the risk of Alzheimer's disease. In this study, we clarified that 17β-estradiol (E2) significantly rescues PC12 neuronal cells from amyloid β protein (Aβ)-induced cell death. We found that the amino acid residues of 25 to 35 (Aβ25-35) were more cytotoxic than the full length protein (Aβ1-40) and these residues induced DNA fragmentation typical for apopto- sis. In addition, E2 was confirmed to inhibit calcium influx and cytochrome c release induced by Aβ25-35. Since these sequential events cause apoptosis, the protective effect of E2 may be exerted not by the direct interaction with Aβ, but by the blockade of the mitochondrial apoptotic pathway induced by Aβ.