期刊
NATURE MEDICINE
卷 10, 期 7, 页码 S2-S9出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm1067
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资金
- NEI NIH HHS [R01 EY016164, R01 EY09024, R01 EY05477] Funding Source: Medline
- NICHD NIH HHS [P01 HD29587] Funding Source: Medline
- NINDS NIH HHS [R01 NS44314, R01 NS43242, R01 NS047456, R01 NS41207, R01 NS44326] Funding Source: Medline
The molecular bases underlying the pathogenesis of neurodegenerative diseases are gradually being disclosed. One problem that investigators face is distinguishing primary from secondary events. Rare, inherited mutations causing familial forms of these disorders have provided important insights into the molecular networks implicated in disease pathogenesis. Increasing evidence indicates that accumulation of aberrant or misfolded proteins, protofibril formation, ubiquitin-proteasome system dysfunction, excitotoxic insult, oxidative and nitrosative stress, mitochondrial injury, synaptic failure, altered metal homeostasis and failure of axonal and dendritic transport represent unifying events in many slowly progressive neurodegenerative disorders.
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