全部文献期刊学位论文会议报纸专利标准年鉴图书|学者科研项目
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作者:Eiichi Tokuda , Itsuki Anzai , Takao Nomura ...
来源:[J].Molecular Neurodegeneration(IF 4.007), 2017, Vol.12 (1)Springer
摘要:Dominant mutations in Cu/Zn-superoxide dismutase ( SOD1 ) gene cause a familial form of amyotrophic lateral sclerosis ( SOD1 -ALS) with accumulation of misfolded SOD1 proteins as intracellular inclusions in spinal motor neurons. Oligomerization of SOD1 via abnormal disulfide cros...
作者:Takashi Miyamoto , Liana Stein , Reuben Thomas ...
来源:[J].Molecular Neurodegeneration(IF 4.007), 2017, Vol.12 (1)Springer
摘要:Hyperexcitability of neuronal networks can lead to excessive release of the excitatory neurotransmitter glutamate, which in turn can cause neuronal damage by overactivating NMDA-type glutamate receptors and related signaling pathways. This process (excitotoxicity) has been i...
作者:Erik Portelius , Niklas Mattsson , Josef Pannee ...
来源:[J].Molecular Neurodegeneration(IF 4.007), 2017, Vol.12 (1)Springer
摘要:Proteolytic degradation of amyloid β (Aβ) peptides has been intensely studied due to the central role of Aβ in Alzheimer’s disease (AD) pathogenesis. While several enzymes have been shown to degrade Aβ peptides, the main pathway of Aβ degradation in vivo is unknown. Cer...
作者:Michal Arbel-Ornath , Eloise Hudry , Josiah R. Boivin ...
来源:[J].Molecular Neurodegeneration(IF 4.007), 2017, Vol.12 (1)Springer
摘要:Amyloid-β oligomers (oAβ) are thought to mediate neurotoxicity in Alzheimer’s disease (AD), and previous studies in AD transgenic mice suggest that calcium dysregulation may contribute to these pathological effects. Even though AD mouse models remain a valuable resource to i...
作者:Maya Ando , Fabienne C. Fiesel , Roman Hudec ...
来源:[J].Molecular Neurodegeneration(IF 4.007), 2017, Vol.12 (1)Springer
摘要:Mutations in PINK1 and PARKIN are the most common causes of recessive early-onset Parkinson’s disease (EOPD). Together, the mitochondrial ubiquitin (Ub) kinase PINK1 and the cytosolic E3 Ub ligase PARKIN direct a complex regulated, sequential mitochondrial quality control. T...
作者:Yi-Ling Liu , Wei-Ting Chen , Yu-Yi Lin ...
来源:[J].Molecular Neurodegeneration(IF 4.007), 2017, Vol.12 (1)Springer
摘要:Microglia mediate amyloid-beta peptide (Aβ)-induced neuroinflammation, which is one of the key events in the pathogenesis of Alzheimer’s disease (AD). Decoy receptor 3 (DcR3)/TNFRSF6B is a pleiotropic immunomodulator that promotes macrophage differentiation toward the M2 ant...
作者:Yu Ohki , Andrea Wenninger-Weinzierl , Alexander Hruscha ...
来源:[J].Molecular Neurodegeneration(IF 4.007), 2017, Vol.12 (1)Springer
摘要:The most frequent genetic cause of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS) is the expansion of a GGGGCC hexanucleotide repeat in a non-coding region of the chromosome 9 open reading frame 72 ( C9orf72) locus. The pathological hallmarks obs...
作者:Clinton Cave , Sungjin Park , Marianeli Rodriguez ...
来源:[J].Molecular Neurodegeneration(IF 4.007), 2017, Vol.12 (1)Springer
摘要:Glycerophosphodiester phosphodiesterase 2 (GDE2) is a six-transmembrane protein that cleaves glycosylphosphatidylinositol (GPI) anchors to regulate GPI-anchored protein activity at the cell surface. In the developing spinal cord, GDE2 utilizes its enzymatic function to regul...
作者:Mang Ching Lai , Anne-Laure Bechy , Franziska Denk ...
来源:[J].Molecular Neurodegeneration(IF 4.007), 2017, Vol.12 (1)Springer
摘要:Genome wide association studies have identified microtubule associated protein tau ( MAPT ) H1 haplotype single nucleotide polymorphisms (SNPs) as leading common risk variants for Parkinson’s disease, progressive supranuclear palsy and corticobasal degeneration. The MAPT ris...
作者:Katarzyna Marta Zoltowska , Masato Maesako , Iryna Lushnikova ...
来源:[J].Molecular Neurodegeneration(IF 4.007), 2017, Vol.12 (1)Springer
摘要:Alzheimer’s disease (AD)-linked protein, presenilin 1 (PS1), is present at the synapse, and the knock-out of presenilin in mice leads to synaptic dysfunction. On the other hand, synaptic activity was shown to influence PS1-dependent generation of distinct amyloid β (Aβ) spec...

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