Early deficits in synaptic mitochondria in an Alzheimer's disease mouse model

By Heng Du, Lan Guo, Shiqiang Yan, A. Sosunov, G. McKhann, Shirley ShiDu Yan. Proceedings of the National Academy of Sciences of the United States of America, 2010

687 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/2a964beed63d981e7f4835401c1f558c0ef05e6b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. S. Gandhi
2. A. Abramov
3. P. Reddy

In Molecular Biology

1. M. Calkins
2. M. Mańczak
3. P. Reddy
4. Plamena R. Angelova
5. S. Gandhi
6. A. Abramov

In Physiology

1. M. Calkins
2. M. Mańczak
3. P. Reddy
4. S. Gandhi
5. A. Abramov
6. Evandro Fei Fang

Citations in the corpus

• Synaptic energy use and supply. (2012, neutral): “…mitochondria are more sensitive to Ab damage than nonsynaptic mitochondria: Ab accumulation occurs earlier in synaptic than in nonsynaptic mitochondria, decreasing mitochondrial trafficking and respiratory function and increasing mitochondrial oxidative stress (Rui et al., 2006; Du et al., 2010).”
• Mitochondrial dysfunction - the beginning of the end in Alzheimer's disease? Separate and synergistic modes of tau and amyloid-β toxicity (2011, background): “…IV activity),antioxidants enzymes Keil et al., 2004 [37] Eckert et al., 2008 [4] Hauptmann et al., 2009 [5] E F F E ROS level, Lipid peroxidation Du et al., 2010 [46] APPS/L / PS1 S t i D t hi it ATP level, MMP E k t t l 2008 [4] C T (KM595/ 596NL; V717I & M141L) ys em c ys rop c neur es ROS…”
• Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms (2017, background): “Synaptic mitochondria may be particularly susceptible to damage by aggregating Aβ because of their high energy demand and robust Ca2+ influx that occur during synaptic activation, particularly at glutamatergic synapses [57].”
• Mechanism of Oxidative Stress in Neurodegeneration (2012, background): “A reduction in complex IV activity has been demonstrated in mitochondria from the hippocampus and platelets of AD patients, as well as in AD animal models and AD cybrid cells in reviewed [37].”
• Role of mitochondrial ROS in the brain: from physiology to neurodegeneration (2018, background): “[27] Du H, Guo L, Yan S, Sosunov AA, McKhann GM, & Yan SS (2010) Early deficits in synaptic mitochondria in an Alzheimer's disease mouse model.”
• 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): “More recently, we (29) and others (30,31) found that Ab reduces total mitochondrial mass; impairs mitochondrial axonal transport, particularly anterograde transport; inhibits synaptic ATP production; and causes synaptic degeneration in neurons affected by AD.”