Editing Reactive oxygen species (section)

===Impairment of cognitive function===
Memory capabilities decline with age, evident in human degenerative diseases such as [[Alzheimer's disease]], which is accompanied by an accumulation of oxidative damage. Current studies demonstrate that the accumulation of ROS can decrease an organism's [[physical fitness|fitness]] because oxidative damage is a contributor to senescence. In particular, the accumulation of oxidative damage may lead to cognitive dysfunction, as demonstrated in a study in which old rats were given mitochondrial [[metabolite]]s and then given [[cognitive tests]]. Results showed that the [[rat]]s performed better after receiving the metabolites, suggesting that the metabolites reduced oxidative damage and improved mitochondrial function.<ref name="pmid11854529">{{Cite journal |display-authors=6 |vauthors=Liu J, Head E, Gharib AM, Yuan W, Ingersoll RT, Hagen TM, Cotman CW, Ames BN |date=February 2002 |title=Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: partial reversal by feeding acetyl-L-carnitine and/or R-alpha -lipoic acid |journal=Proceedings of the National Academy of Sciences of the United States of America |volume=99 |issue=4 |pages=2356–2361 |bibcode=2002PNAS...99.2356L |doi=10.1073/pnas.261709299 |pmc=122369 |pmid=11854529 |doi-access=free}}</ref> Accumulating oxidative damage can then affect the efficiency of mitochondria and further increase the rate of ROS production.<ref name="pmid1355616">{{Cite journal |vauthors=Stadtman ER |date=August 1992 |title=Protein oxidation and aging |url=https://zenodo.org/record/1230934 |journal=Science |volume=257 |issue=5074 |pages=1220–1224 |bibcode=1992Sci...257.1220S |doi=10.1126/science.1355616 |pmid=1355616}}</ref> The accumulation of oxidative damage and its implications for aging depends on the particular [[tissue (biology)|tissue]] type where the damage is occurring. Additional experimental results suggest that oxidative damage is responsible for age-related decline in [[brain]] functioning. Older [[gerbil]]s were found to have higher levels of oxidized protein in comparison to younger gerbils. Treatment of old and young [[mice]] with a [[spin trapping]] compound caused a decrease in the level of oxidized proteins in older gerbils but did not have an effect on younger gerbils. In addition, older gerbils performed cognitive tasks better during treatment but ceased functional capacity when treatment was discontinued, causing oxidized protein levels to increase. This led researchers to conclude that oxidation of cellular proteins is potentially important for brain function.<ref name="CarneyStarke-Reed1991">{{Cite journal |vauthors=Carney JM, Starke-Reed PE, Oliver CN, Landum RW, Cheng MS, Wu JF, Floyd RA |date=May 1991 |title=Reversal of age-related increase in brain protein oxidation, decrease in enzyme activity, and loss in temporal and spatial memory by chronic administration of the spin-trapping compound N-tert-butyl-alpha-phenylnitrone |journal=Proceedings of the National Academy of Sciences of the United States of America |volume=88 |issue=9 |pages=3633–3636 |bibcode=1991PNAS...88.3633C |doi=10.1073/pnas.88.9.3633 |pmc=51506 |pmid=1673789 |doi-access=free}}</ref>