Mitochondrial Aβ: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease

By C. Caspersen, Ning Wang, Jun Yao, A. Sosunov, X. Chen, J. Lustbader, Hong Wei Xu, D. Stern, G. McKhann, Shi Du Yan. 2005

680 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/267fe31b12c35ac4e906c580b4fb9afc66f4d9b0

How researchers see this paper

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

In Genetics

1. K. Johnson
2. Barry Halliwell

In Molecular Biology

1. P. Reddy
2. M. Beal
3. A. Abramov
4. S. Gandhi
5. M. Mańczak
6. E. K. Kim
7. E. Choi
8. K. Johnson

In Physiology

1. P. Reddy
2. M. Beal
3. A. Abramov
4. S. Gandhi
5. M. Mańczak
6. E. K. Kim
7. E. Choi
8. Barry Halliwell

Citations in the corpus

• Accumulation of Amyloid Precursor Protein in the Mitochondrial Import Channels of Human Alzheimer’s Disease Brain Is Associated with Mitochondrial Dysfunction (2006, result): “In support of others studies (Hirai et al., 2001; Caspersen et al., 2005; Crouch et al., 2005; Manczak et al., 2006), in the present study, we also observed A species in the mitochondria of AD brain (Fig.”
• Oxidative stress and neurodegeneration: where are we now? (2006, background): “In addition, aggregating Abs raise intracellular Ca2+, increase NOX activity in astrocytes and directly produce ROS (Barnham et al. 2004; Abramov and Duchen 2005; Caspersen et al. 2005; Sultana et al. 2006).”
• Pathological roles of MAPK signaling pathways in human diseases. (2010, background): “Although most Aβ proteins including Aβ42 and Aβ40 are secreted extracellularly, intracellular Aβ42 has been shown to initiate mitochondrial oxidative stress and has been implicated in the pathogenesis of AD [26,27].”
• Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease. (2008, background): “The loss of synapses, synaptic damage, and mitochondrial oxidative damage have been reported as early events in AD progression [1–4,15,16].”
• Mitochondria are a direct site of A beta accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progression. (2006, methodology): “Our study mainly focused on measuring hydrogen peroxide radicals, carbonyl proteins and cytochrome oxidase activity in the mitochondria, because mitochondria are a major source of free radicals, and it has been proposed that Ab induces free radicals in the mitochondria (20,22,32, 40 ).”
• Mitochondrial dysfunction - the beginning of the end in Alzheimer's disease? Separate and synergistic modes of tau and amyloid-β toxicity (2011, background): “In another transgenic mouse model, APPS/L, which combines the Swedish (K670M/N671L) with the London (V717I) mutation in the human APP gene, an early energy dysfunction was found as shown by a decreased mitochondrial membrane potential as well as decreased ATP levels at 3 months of age, when Aβ level”