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Beta-amyloid (1-42)-induced learning and memory deficits in mice: involvement of oxidative burdens in the hippocampus and cerebral cortex.
Behav Brain Res. 2004 Dec 06; 155(2):185-96.BB

Abstract

We have demonstrated that oxidative stress is involved, at least in part, in beta-amyloid protein (Abeta)-induced neurotoxicity in vivo [Eur. J. Neurosci. 1999;11:83-90; Neuroscience 2003;119:399-419]. However, mechanistic links between oxidative stress and memory loss in response to Abeta remain elusive. In the present study, we examined whether oxidative stress contributes to the memory deficits induced by intracerebroventricular injection of Abeta (1-42) in mice. Abeta (1-42)-induced memory impairments were observed, as measured by the water maze and passive avoidance tests, although these impairments were not found in Abeta (40-1)-treated mice. Treatment with antioxidant alpha-tocopherol significantly prevented memory impairment induced by Abeta (1-42). Increased activities of the cytosolic Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and mitochondrial Mn-superoxide dismutase (Mn-SOD) were observed in the hippocampus and cerebral cortex of Abeta (1-42)-treated animals, as compared with Abeta (40-1)-treated mice. The induction of Cu,Zn-SOD was more pronounced than that of Mn-SOD after Abeta (1-42) insult. However, the concomitant induction of glutathione peroxidase (GPX) in response to significant increases in SOD activity was not seen in animals treated with Abeta (1-42). Furthermore, glutathione reductase (GRX) activity was only increased at 2h after Abeta (1-42) injection. Production of malondialdehyde (lipid peroxidation) and protein carbonyl (protein oxidation) remained elevated at 10 days post-Abeta (1-42), but the antioxidant alpha-tocopherol significantly prevented these oxidative stresses. Therefore, our results suggest that the oxidative stress contributes to the Abeta (1-42)-induced learning and memory deficits in mice.

Authors+Show Affiliations

Department of Psychiatry, Pundang Jesaeng Hospital, Daejin Medical Center, Seongnam, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15364477

Citation

Jhoo, Jin Hyeong, et al. "Beta-amyloid (1-42)-induced Learning and Memory Deficits in Mice: Involvement of Oxidative Burdens in the Hippocampus and Cerebral Cortex." Behavioural Brain Research, vol. 155, no. 2, 2004, pp. 185-96.
Jhoo JH, Kim HC, Nabeshima T, et al. Beta-amyloid (1-42)-induced learning and memory deficits in mice: involvement of oxidative burdens in the hippocampus and cerebral cortex. Behav Brain Res. 2004;155(2):185-96.
Jhoo, J. H., Kim, H. C., Nabeshima, T., Yamada, K., Shin, E. J., Jhoo, W. K., Kim, W., Kang, K. S., Jo, S. A., & Woo, J. I. (2004). Beta-amyloid (1-42)-induced learning and memory deficits in mice: involvement of oxidative burdens in the hippocampus and cerebral cortex. Behavioural Brain Research, 155(2), 185-96.
Jhoo JH, et al. Beta-amyloid (1-42)-induced Learning and Memory Deficits in Mice: Involvement of Oxidative Burdens in the Hippocampus and Cerebral Cortex. Behav Brain Res. 2004 Dec 6;155(2):185-96. PubMed PMID: 15364477.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Beta-amyloid (1-42)-induced learning and memory deficits in mice: involvement of oxidative burdens in the hippocampus and cerebral cortex. AU - Jhoo,Jin Hyeong, AU - Kim,Hyoung-Chun, AU - Nabeshima,Toshitaka, AU - Yamada,Kiyofumi, AU - Shin,Eun-Joo, AU - Jhoo,Wang-Kee, AU - Kim,Wookyung, AU - Kang,Kee-Seok, AU - Jo,Sangmee Ahn, AU - Woo,Jong Inn, PY - 2004/02/06/received PY - 2004/04/13/revised PY - 2004/04/13/accepted PY - 2004/9/15/pubmed PY - 2005/1/14/medline PY - 2004/9/15/entrez SP - 185 EP - 96 JF - Behavioural brain research JO - Behav Brain Res VL - 155 IS - 2 N2 - We have demonstrated that oxidative stress is involved, at least in part, in beta-amyloid protein (Abeta)-induced neurotoxicity in vivo [Eur. J. Neurosci. 1999;11:83-90; Neuroscience 2003;119:399-419]. However, mechanistic links between oxidative stress and memory loss in response to Abeta remain elusive. In the present study, we examined whether oxidative stress contributes to the memory deficits induced by intracerebroventricular injection of Abeta (1-42) in mice. Abeta (1-42)-induced memory impairments were observed, as measured by the water maze and passive avoidance tests, although these impairments were not found in Abeta (40-1)-treated mice. Treatment with antioxidant alpha-tocopherol significantly prevented memory impairment induced by Abeta (1-42). Increased activities of the cytosolic Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and mitochondrial Mn-superoxide dismutase (Mn-SOD) were observed in the hippocampus and cerebral cortex of Abeta (1-42)-treated animals, as compared with Abeta (40-1)-treated mice. The induction of Cu,Zn-SOD was more pronounced than that of Mn-SOD after Abeta (1-42) insult. However, the concomitant induction of glutathione peroxidase (GPX) in response to significant increases in SOD activity was not seen in animals treated with Abeta (1-42). Furthermore, glutathione reductase (GRX) activity was only increased at 2h after Abeta (1-42) injection. Production of malondialdehyde (lipid peroxidation) and protein carbonyl (protein oxidation) remained elevated at 10 days post-Abeta (1-42), but the antioxidant alpha-tocopherol significantly prevented these oxidative stresses. Therefore, our results suggest that the oxidative stress contributes to the Abeta (1-42)-induced learning and memory deficits in mice. SN - 0166-4328 UR - https://www.unboundmedicine.com/medline/citation/15364477/Beta_amyloid__1_42__induced_learning_and_memory_deficits_in_mice:_involvement_of_oxidative_burdens_in_the_hippocampus_and_cerebral_cortex_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166432804001536 DB - PRIME DP - Unbound Medicine ER -