TY - JOUR
T1 - RNA oxidation in Alzheimer and Parkinson diseases
AU - Nunomura, Akihiko
AU - Perry, George
AU - Zhang, Jing
AU - Montine, Thomas J.
AU - Takeda, Atsushi
AU - Chiba, Shigeru
AU - Smith, Mark A.
PY - 1999/1/1
Y1 - 1999/1/1
N2 - In Alzheimer and Parkinson diseases, oxidative alterations, affecting lipids, proteins, and DNA, have been described. Using an in situ approach to identify 8-hydroxyguanosine, an oxidized nucleoside, we recently identified RNA as a major target of oxidation in Alzheimer and Parkinson diseases as well as Down syndrome, where premature Alzheimer-like neuropathology is invariably found. RNA oxidation is localized to the neuronal populations potentially affected in these diseases. Together with the known mitochondrial dysfunction in Alzheimer and Parkinson diseases, the cytoplasmic predominance of neuronal 8-hydroxyguanosine supports mitochondria as the most likely source of reactive oxygen responsible for RNA oxidation. The consequence of oxidatively damaged RNA is not fully understood; however, the potential of oxidized RNA to cause errors in translation indicates a metabolic abnormality in neurodegenerative diseases.
AB - In Alzheimer and Parkinson diseases, oxidative alterations, affecting lipids, proteins, and DNA, have been described. Using an in situ approach to identify 8-hydroxyguanosine, an oxidized nucleoside, we recently identified RNA as a major target of oxidation in Alzheimer and Parkinson diseases as well as Down syndrome, where premature Alzheimer-like neuropathology is invariably found. RNA oxidation is localized to the neuronal populations potentially affected in these diseases. Together with the known mitochondrial dysfunction in Alzheimer and Parkinson diseases, the cytoplasmic predominance of neuronal 8-hydroxyguanosine supports mitochondria as the most likely source of reactive oxygen responsible for RNA oxidation. The consequence of oxidatively damaged RNA is not fully understood; however, the potential of oxidized RNA to cause errors in translation indicates a metabolic abnormality in neurodegenerative diseases.
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U2 - 10.1089/rej.1.1999.2.227
DO - 10.1089/rej.1.1999.2.227
M3 - Article
AN - SCOPUS:0032718289
VL - 2
SP - 227
EP - 230
JO - Rejuvenation Research
JF - Rejuvenation Research
SN - 1549-1684
IS - 3
ER -