2006
DOI: 10.1016/j.brainresrev.2006.04.003
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A new insight on Al-maltolate-treated aged rabbit as Alzheimer's animal model

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Cited by 80 publications
(33 citation statements)
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“…This could be due to the reduced axonal mitochondria turnover, disruption of Golgi and reduction of synaptic vesicles induced by Al exposure which results in release of oxidative products like MDA and carbonyls within the neurons (Bharathi et al, 2006), this is already supported by the present study.…”
Section: Oxidative Stress Markerssupporting
confidence: 78%
“…This could be due to the reduced axonal mitochondria turnover, disruption of Golgi and reduction of synaptic vesicles induced by Al exposure which results in release of oxidative products like MDA and carbonyls within the neurons (Bharathi et al, 2006), this is already supported by the present study.…”
Section: Oxidative Stress Markerssupporting
confidence: 78%
“…As a result, activated SOD enzyme readily converts the superoxide anion into hydrogen peroxide (H 2 O 2 ). However, deactivated catalase could not convert the H 2 O 2 into water and oxygen that further leads to generation of hydroxyl radical ion [44]. These factors contribute towards oxidative stress that ultimately leads to neurodegeneration.…”
Section: Discussionmentioning
confidence: 99%
“…Previously, Al has been widely used as a cell death-inducing agent to mimic cell degeneration pathology, especially in AD [8,9,26]. Moreover, it has been suggested that Al-induced apoptotic changes, oxidative stress, and axonal transport disruption are linked in a way that promotes neurodegeneration [27][28][29]. If similar regulatory mechanisms are indeed recapitulated, Al-induced cellular toxicity might serve as a useful model to understand the molecular underpinnings that underlie neuronal cell death during neurodegeneration.…”
Section: Discussionmentioning
confidence: 99%