Amyloid-β overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins
By Xinglong Wang, B. Su, S. Siedlak, P. Moreira, H. Fujioka, Yang Wang, G. Casadesus, Xiongwei Zhu. Proceedings of the National Academy of Sciences of the United States of America, 2008
844 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/bf404b79e2a1a5fc1ee28bacb65e24271be9ceae
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Clinical Biochemistry
In Molecular Biology
In Physiology
Citations in the corpus
- Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “Mitochondrial dysfunction in AD has been demonstrated the association with the imbalance of mitochondrial fission and fusion (Bonda et al., 2010; Wang et al., 2008).”
- Mitochondrial dynamics–fusion, fission, movement, and mitophagy–in neurodegenerative diseases (2009, background): “The same group, however, found that APP over-expression in M17 neuroblastoma cells resulted in predominantly fragmented mitochondria, decreased levels of Drp1 and OPA1, and a defect in neuronal differentiation (72).”
- Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage. (2011, background): “(32,33), who also reported increased Fis1 in AD patients, although the progression of AD in their patients was not specified.”
- Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease (2012, background): “As expected, such mitochondrial deficits became more severe in M17 cells expressing the familial AD-causing Swedish APP mutation [96].”
- Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease. (2011, result): “Recently, this idea has been supported with studies of M17 cells that were found to overexpress mutant AbPP (22,23).”
- Mechanism of Oxidative Stress in Neurodegeneration (2012, background): “Fragmented mitochondria are seen in AD hippocampus in association with a downregulation of mitochondrial fusion proteins (MFN-1, MFN-2, OPA-1), with an increase in expression of the mitochondrial fission protein Fis-1 [47].”
- Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology. (2010, background): “The authors concluded that AβPP, through Aβ production, causes an imbalance of mitochondrial fission/fusion that results in mitochondrial fragmentation and abnormal distribution, which contributes to mitochondrial and neuronal dysfunction [39].”
- Mitochondrial dysfunction - the beginning of the end in Alzheimer's disease? Separate and synergistic modes of tau and amyloid-β toxicity (2011, background): “M17 Systemic Retinoic acid- induced differentiation ATP level, MMP ROS level Mitochondrial dynamics Wang et al 2008 [39] E P E N (APPwt & APPsw) , (fusion/fission) and morphology/ distribution abnormalities ., APPSw (KM595/ 596NL) Systemic Synaptic transmission & LTP mitochondrial hsp70, subunits…”
- Impaired Balance of Mitochondria Fission and Fusion in Alzheimer Disease (2009, methodology): “After blocking with 10% nonfat dry milk, primary and secondary antibodies were applied as previously described (Wang et al., 2008a) and the blots developed with Immobilon Western Chemiluminescent HRP Substrate (Millipore).”
- Amyloid β-based therapy for Alzheimer’s disease: challenges, successes and future (2023, background): “Thus, restoration of mitochondrial fission rescued APP- or Aβ-induced mitochondrial abnormality and neuronal damage.(200,201) Only 1% of mitochondrial proteins are synthesized in the mitochondria itself.”