2011
DOI: 10.3233/jad-2011-110423
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Abstract: Mitochondrial dysfunction is observed in Alzheimer's disease (AD) brain and peripheral tissues. Amyloid-β (Aβ) peptides are known to interact with several proteins inside the mitochondria, leading to mitochondrial dysfunction. Recent studies have provided substantial evidence that mitochondria serve as direct targets for Aβ-mediated neuronal toxicity. The observations that Aβ progressively accumulates in cortical mitochondria from AD patients and transgenic AD type mouse models suggest the role of mitochondria… Show more

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Cited by 49 publications
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References 57 publications
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“…MTs have been imaged moving in and out of dendritic spines in the seconds to minutes timeframe, and are hypothesized to play a role in spine alterations in response to activity (Hoogenraad and Akhmanova, 2010). Finally, BMS-241027 may be improving neuronal function through an influence on signaling pathways, protein clearance, or mitochondrial function, which would then lead to later improvements in MT dynamics (Michaelis et al, 2005;Shemesh et al, 2008;Vossel et al, 2010;Gardiner et al, 2011;Lee et al, 2011;Silva et al, 2011).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…MTs have been imaged moving in and out of dendritic spines in the seconds to minutes timeframe, and are hypothesized to play a role in spine alterations in response to activity (Hoogenraad and Akhmanova, 2010). Finally, BMS-241027 may be improving neuronal function through an influence on signaling pathways, protein clearance, or mitochondrial function, which would then lead to later improvements in MT dynamics (Michaelis et al, 2005;Shemesh et al, 2008;Vossel et al, 2010;Gardiner et al, 2011;Lee et al, 2011;Silva et al, 2011).…”
Section: Discussionmentioning
confidence: 99%
“…These molecules are cytotoxic to dividing cells by interfering with MT-dependent chromosome separation. On the other hand, MT stabilizers are neuroprotective for A␤-mediated toxicity (Michaelis et al, 2002;Silva et al, 2011), enhance neurite outgrowth (Sengottuvel et al, 2011), and reduce deficits induced by tau-P301L transfection (Shemesh and Spira, 2011) in cultured neurons. In vivo, paclitaxel (Taxol), which does not have good brain penetration, improves axonal transport rate, MT numbers, and motor function in a spinal cord tauopathy model (Zhang et al, 2005).…”
Section: Introductionmentioning
confidence: 99%
“…In this latter study the mitochondrial motility alterations were associated to increased oxidative stress and could be partially reverted by treatment with mitochondrial targeted antioxidants . The mechanisms of Aβ-induced altered mitochondrial movement are not well understood, but it has been recently described that Aβ peptides decreased acetylated tubulin levels and tau hyperphosphorilation, causing disturbances in microtubule dynamics and alterations in macroautophagy, whereas taxol treatment restored microtubule network and reduced Aβ oligomers accumulation (Silva et al, 2011). These findings support the notion that in AD, Aβ can alter mitochondrial dynamics by inducing post-translational modifications of the proteins involved in fission and fusion, leading to an enhancement of fission and also disturbing the tracks along which mitochondria move in the cell, which would in turn alter the delivery of functional mitochondria to neuronal axons and dendrites.…”
Section: In Alzheimer´s Diseasementioning
confidence: 99%
“…Until now, several MT-binding compounds have been tested and the studies carried out have provided proof of concept that MT-binding agents or compounds with the ability to stabilize MTs may have therapeutic potential for the treatment of Alzheimer's disease and other neurodegenerative diseases [Michaelis et al 2002Silva et al 2011;Nelson, 2005;Butler et al 2007]. …”
Section: Microtubule-stabilizing Compoundsmentioning
confidence: 99%