TY - JOUR
T1 - Mitochondrion-specific antioxidants as drug treatments for alzheimer disease
AU - Palacios, Hector H.
AU - Yendluri, Bharat B.
AU - Parvathaneni, Kalpana
AU - Shadlinski, Vagif B.
AU - Obrenovich, Mark E.
AU - Leszek, Jerzy
AU - Gokhman, Dmitry
AU - Gasiorowski, Kazimierz
AU - Bragin, Valentin
AU - Aliev, Gjumrakch
PY - 2011
Y1 - 2011
N2 - Age-related dementias such as Alzheimer disease (AD) have been linked to vascular disorders like hypertension, diabetes and atherosclerosis. These risk factors cause ischemia, inflammation, oxidative damage and consequently reperfusion, which is largely due to reactive oxygen species (ROS) that are believed to induce mitochondrial damage. At higher concentrations, ROS can cause cell injury and death which occurs during the aging process, where oxidative stress is incremented due to an accelerated generation of ROS and a gradual decline in cellular antioxidant defense mechanisms. Neuronal mitochondria are especially vulnerable to oxidative stress due to their role in energy supply and use, causing a cascade of debilitating factors such as the production of giant and/or vulnerable young mitochondrion who's DNA has been compromised. Therefore, mitochondria specific antioxidants such as acetyl-L-carnitine and R-alphalipoic acid seem to be potential treatments for AD. They target the factors that damage mitochondria and reverse its effect, thus eliminating the imbalance seen in energy production and amyloid beta oxidation and making these antioxidants very powerful alternate strategies for the treatment of AD.
AB - Age-related dementias such as Alzheimer disease (AD) have been linked to vascular disorders like hypertension, diabetes and atherosclerosis. These risk factors cause ischemia, inflammation, oxidative damage and consequently reperfusion, which is largely due to reactive oxygen species (ROS) that are believed to induce mitochondrial damage. At higher concentrations, ROS can cause cell injury and death which occurs during the aging process, where oxidative stress is incremented due to an accelerated generation of ROS and a gradual decline in cellular antioxidant defense mechanisms. Neuronal mitochondria are especially vulnerable to oxidative stress due to their role in energy supply and use, causing a cascade of debilitating factors such as the production of giant and/or vulnerable young mitochondrion who's DNA has been compromised. Therefore, mitochondria specific antioxidants such as acetyl-L-carnitine and R-alphalipoic acid seem to be potential treatments for AD. They target the factors that damage mitochondria and reverse its effect, thus eliminating the imbalance seen in energy production and amyloid beta oxidation and making these antioxidants very powerful alternate strategies for the treatment of AD.
KW - Alzheimer disease
KW - Antioxidants
KW - Mitochondria
KW - Oxidative stress
KW - Reactive oxygen species
UR - https://www.scopus.com/pages/publications/79551673088
U2 - 10.2174/187152711794480474
DO - 10.2174/187152711794480474
M3 - Article
C2 - 21222631
AN - SCOPUS:79551673088
SN - 1871-5273
VL - 10
SP - 149
EP - 162
JO - CNS and Neurological Disorders - Drug Targets
JF - CNS and Neurological Disorders - Drug Targets
IS - 2
ER -