作者: Marius Heitzer , Sarah Kaiser , Mithila Kanagaratnam , Adib Zendedel , Philipp Hartmann
DOI: 10.1007/S12035-017-0391-Z
关键词: Amyotrophic lateral sclerosis 、 Caspase 1 、 Immunology 、 Inflammasome 、 Spinal cord 、 Neuroprotection 、 Neuroinflammation 、 Endocrinology 、 Lumbar Spinal Cord 、 Internal medicine 、 SOD1 、 Medicine
摘要: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease manifested by the progressive loss of upper and lower motoneurons. The pathomechanism ALS complex not yet fully understood. Neuroinflammation believed to significantly contribute progression. Inflammasome activation was recently shown in spinal cord human sporadic patients SOD1(G93A) mouse model for ALS. In present study, we investigated neuroprotective anti-inflammatory effects 17β-estradiol (E2) treatment pre-symptomatic symptomatic male mice. Symptomatic mice with E2 substitution exhibited improved motor performance correlating an increased survival motoneurons lumbar cord. Expression NLRP3 inflammasome proteins levels activated caspase 1 mature interleukin beta were reduced supplemented E2.