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.

By M. Mańczak, T. Anekonda, E. Henson, Byung S Park, J. Quinn, P. Reddy. Human Molecular Genetics, 2006

1,143 citations recorded by the source corpus.

Subfields: Molecular Biology, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/006b5de909df9fc4679fb089899d8a74f53ee906

How researchers see this paper

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

In Molecular Biology

1. D. C. Chan
2. Hsiuchen Chen
3. M. Beal
4. P. Reddy
5. E. Trushina
6. E. Tönnies
7. C. Zhong
8. Zhichun Chen

In Pharmacology

1. M. Beal
2. P. Reddy
3. Yan Zhao
4. Baolu Zhao
5. M. Calkins
6. M. Mańczak

In Physiology

1. P. Reddy
2. M. Calkins
3. M. Beal
4. E. Trushina
5. E. Tönnies
6. M. Mańczak
7. Yan Zhao
8. Baolu Zhao

Citations in the corpus

• Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease. (2011, methodology): “Protein changes in mitochondrial proteins (Drp1, Fis1, Mfn1, Mfn2 and Opa1) were also probed with western blot analysis (Fig.”
• Mitochondrial Glutathione, a Key Survival Antioxidant (2009, background): “Current evidence indicates that targeting of Ab to intracellular sites, most notably mitochondria, causes oxidative stress, mitochondrial dysfunction, and cell death (80, 91).”
• 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, methodology): “Recently, we (22) and others (23–25) found both monomeric and oligomeric Ab in mitochondria, in the neurons affected by AD, and mitochondrial- Ab—interact with mitochondrial proteins, increase free radicals production, decrease cytochrome c oxidase activity, inhibit mitochondrial ATP and damage mito”
• Mitochondria, oxidative stress and neurodegeneration. (2012, background): “In brains of AD patients and transgenic mouse models, ßamyloid protein (Aß) interacts with binding alcohol dehydrogenase protein (ABAD), a mitochondrial-matrix protein, causing mitochondrial oxidative damage and impaired activity of respiratory complexes [72].”
• Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, positive): “With this regard, in vivo and in vitro experiments have shown that soluble Ab impairs mitochondria metabolism by decreasing cytochrome oxidase activity and increasing hydrogen peroxide generation (Manczak et al., 2006).”
• Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease. (2008, background): “Two recent studies found that APP directly interacts with mitochondrial proteins [1,83].”
• Accumulation of Amyloid Precursor Protein in the Mitochondrial Import Channels of Human Alzheimer’s Disease Brain Is Associated with Mitochondrial Dysfunction (2006, background): “Mitochondrial accumulation of APP is associated with decreased cytochrome c oxidase activity and increased levels of H2O2 in mitochondria Reduced mitochondrial cytochrome c oxidase activity and increased oxidative stress have been associated with the pathogenesis of AD (Parker, 1991; Maurer et al., ”
• Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases (2006, positive): “Two other groups have also reported that Aβ interacts with mitochondria, inhibiting cytochrome oxidase activity and increasing free-radical generatio”