Key Role of Mitochondria in Alzheimer's Disease Synaptic Dysfunction

被引:38
|
作者
Cavallucci, Virve [1 ]
Ferraina, Caterina [2 ]
D'Amelio, Marcello [1 ,3 ]
机构
[1] IRCCS Fdn Santa Lucia, Dept Expt Neurosci, I-00143 Rome, Italy
[2] European Brain Res Inst, Pharmacol Synapt Plast Unit, I-00143 Rome, Italy
[3] Univ Campus Biomed, Lab Mol Neurosci, I-00128 Rome, Italy
关键词
Cell death; mitochondria dynamics; apoptosis; ATP production; neurotransmitter release; synaptic function; NERVE GROWTH-FACTOR; PERMEABILITY TRANSITION PORE; AMYLOID PRECURSOR PROTEIN; DYNAMIN-RELATED PROTEIN; CYTOCHROME-C RELEASE; DIFFERENTIATION-ASSOCIATED PROTEIN-1; NEUROTROPHIC FACTOR BDNF; DEPENDENT ANION CHANNEL; LONG-TERM DEPRESSION; ENDOPLASMIC-RETICULUM;
D O I
10.2174/1381612811319360005
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Neuronal transmission and functional synapses require mitochondria, which are mainly involved in the generation of energy (ATP and NAD(+)), regulation of cell signaling and calcium homeostasis. Particularly intriguing is emerging data suggesting the relationship between mitochondria and neurotrophic factors that can act at the synaptic level promoting neuronal transmission and plasticity. On the other hand, disturbances in mitochondrial functions might contribute to impaired synaptic transmission and neuronal degeneration in Alzheimer's Disease and other chronic and acute neurodegenerative disorders. Here, we review the molecular mediators controling mitochondrial function and their impact on synaptic dysfunction associated with the pathogenesis of Alzheimer's Disease.
引用
收藏
页码:6440 / 6450
页数:11
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