- Email: [email protected]
EXTRA VIRGIN OLIVE OIL DIET ATTENUATES AMYLOID AND TAU PATHOLOGY AND IMPROVES COGNITIVE FUNCTION IN ALZHEIMER’S DISEASE MICE
P270
Poster Presentations: Sunday, July 16, 2017
age, mean serum 25(OH)D was 4.52 ng/mL (s¼1.19, 2 outliers removed), confirming VitD deficiency. At 12 months of age, lower serum 25(OH)D was observed in the group treated with memantine only (p<0.05) and in the group receiving no treatment (p<0.0001), compared to the group receiving memantine and VitD supplementation. After adjusting for differences in physical ability, anxiety, and weight, mice receiving memantine only or memantine with VitD supplementation performed better than mice receiving no treatment (p<0.05, d¼0.98; p<0.05, d¼1.07), as measured by proximity to the target region during the MWM probe trial. No differences were found between mice receiving memantine only or memantine with VitD supplementation. Conclusions: 3-month treatment using memantine with or without VitD supplementation improves cognition in chronically VitD deficient APPSwe/PS1-dE9 mice. The combined treatment of memantine and VitD supplementation in VitD deficient mice did not provide further cognitive improvement over memantine alone.
Compared with controls, mice receiving the EVOO-rich diet had an amelioration of their behavioral deficits, and a significant increase in the steady state levels of synaptophysin, a protein marker of synaptic integrity. In addition, they had a significant reduction in insoluble Ab peptide levels and deposition, lower amount of phosphorylated tau protein at specific epitopes, which were secondary to an activation of the cell autophagic machinery. Conclusions: Taken together, our findings support a beneficial effect of EVOO consumption on all major features of the AD phenotype (behavioral deficits, synaptic pathology, Ab and tau neuropathology), and demonstrate that autophagy activation is the mechanism underlying this biological action.
P1-084
LONG-TERM DRINKING INDUCES TAU HYPERPHOSPHORYLATION AND COGNITIVE DEFICIT
Huang Fang, Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Contact e-mail: [email protected]
P1-083
EXTRA VIRGIN OLIVE OIL DIET ATTENUATES AMYLOID AND TAU PATHOLOGY AND IMPROVES COGNITIVE FUNCTION IN ALZHEIMER’S DISEASE MICE
Elisabetta Lauretti1, Luigi Iuliano2, Domenico Pratico1, 1Lewis Katz School of Medicine Temple University, Philadelphia, PA, USA; 2Universita Degli Studi di Roma “La Sapienza”, Rome, Italy. Contact e-mail: [email protected] Background: Several epidemiological studies have suggested
that the Mediterranean diet protects the brain from the detrimental effect of aging and that extra virgin olive oil, its principal component, may help to reduce the risk of developing Alzheimer’s disease and other forms of dementia. However, the mechanisms involved in this protective action is still incompletely understood. Methods: 6 month-old 3xTg mice received either regular chow diet (n¼ 11) or chow diet supplemented with EVOO (n¼10) for 6 months. We investigated the effect of EVOO on amyloid beta deposition, tau phosphorylation, memory and learning, and synaptic integrity. Results:
Background: Multiple lines of evidence suggests that brain tissues in Alzheimer disease (AD) patients are exposed to oxidative stress during the development of the disease. Alcohol has been reported to be associated with neurodegenerative diseases via oxidative stress. However, effect of alcohol on AD mechanism is less known. In the present study, we investigated the effect of long-term drinking induced oxidative stress injury on AD mechanism in the brain of rats. Methods: Adult male SD rats were given by gavage once a day with 4ml/kg of drinking alcohol for 30 days as the model group, or normal saline with the same volume as the control group, or simultaneous intra gastric treatment, and intra gastric treatment with Melatonin (40ug/day) as treatment group. Memory and cognition were access by Morris Water Maze after the final intra gastric. After sacrifice, western blot and ELISA were carried out to check multiple protein levels and activities related to oxidative stress AD pathology. Results: Long-term drinking leads to a decrease of PP2A activity, an increase of GSK-3b activity, a decrease of SOD activity, an increase of MDA level, and abnormal hyperphosphorylation of tau at serine 199, serine 396 and serine 404 in both hippocampus and cortex. Morris water maze behavioral test revealed that alcohol treated rats induced spatial reference memory and memory consolidation deficits. Treatment of melatonin, an inhibitor of oxidative stress, attenuates the decrease of PP2A activity, increase of GSK-3b activity, decrease of SOD activity, increase of MDA level and tau hyperphosphorylation. Conclusions: These findings suggest that longterm drinking induced oxidative stress leads to GSK-3b activation, PP2A inhibition, and then tau hyperphosphorylation and cognitive deficit. Melatonin, an inhibitor of oxidative stress, attenuated these changes to some extent. Our study provided a clear insight, for the treatment of AD and other oxidative stress related pathology.
Poster Presentations: Sunday, July 16, 2017
age, mean serum 25(OH)D was 4.52 ng/mL (s¼1.19, 2 outliers removed), confirming VitD deficiency. At 12 months of age, lower serum 25(OH)D was observed in the group treated with memantine only (p<0.05) and in the group receiving no treatment (p<0.0001), compared to the group receiving memantine and VitD supplementation. After adjusting for differences in physical ability, anxiety, and weight, mice receiving memantine only or memantine with VitD supplementation performed better than mice receiving no treatment (p<0.05, d¼0.98; p<0.05, d¼1.07), as measured by proximity to the target region during the MWM probe trial. No differences were found between mice receiving memantine only or memantine with VitD supplementation. Conclusions: 3-month treatment using memantine with or without VitD supplementation improves cognition in chronically VitD deficient APPSwe/PS1-dE9 mice. The combined treatment of memantine and VitD supplementation in VitD deficient mice did not provide further cognitive improvement over memantine alone.
Compared with controls, mice receiving the EVOO-rich diet had an amelioration of their behavioral deficits, and a significant increase in the steady state levels of synaptophysin, a protein marker of synaptic integrity. In addition, they had a significant reduction in insoluble Ab peptide levels and deposition, lower amount of phosphorylated tau protein at specific epitopes, which were secondary to an activation of the cell autophagic machinery. Conclusions: Taken together, our findings support a beneficial effect of EVOO consumption on all major features of the AD phenotype (behavioral deficits, synaptic pathology, Ab and tau neuropathology), and demonstrate that autophagy activation is the mechanism underlying this biological action.
P1-084
LONG-TERM DRINKING INDUCES TAU HYPERPHOSPHORYLATION AND COGNITIVE DEFICIT
Huang Fang, Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Contact e-mail: [email protected]
P1-083
EXTRA VIRGIN OLIVE OIL DIET ATTENUATES AMYLOID AND TAU PATHOLOGY AND IMPROVES COGNITIVE FUNCTION IN ALZHEIMER’S DISEASE MICE
Elisabetta Lauretti1, Luigi Iuliano2, Domenico Pratico1, 1Lewis Katz School of Medicine Temple University, Philadelphia, PA, USA; 2Universita Degli Studi di Roma “La Sapienza”, Rome, Italy. Contact e-mail: [email protected] Background: Several epidemiological studies have suggested
that the Mediterranean diet protects the brain from the detrimental effect of aging and that extra virgin olive oil, its principal component, may help to reduce the risk of developing Alzheimer’s disease and other forms of dementia. However, the mechanisms involved in this protective action is still incompletely understood. Methods: 6 month-old 3xTg mice received either regular chow diet (n¼ 11) or chow diet supplemented with EVOO (n¼10) for 6 months. We investigated the effect of EVOO on amyloid beta deposition, tau phosphorylation, memory and learning, and synaptic integrity. Results:
Background: Multiple lines of evidence suggests that brain tissues in Alzheimer disease (AD) patients are exposed to oxidative stress during the development of the disease. Alcohol has been reported to be associated with neurodegenerative diseases via oxidative stress. However, effect of alcohol on AD mechanism is less known. In the present study, we investigated the effect of long-term drinking induced oxidative stress injury on AD mechanism in the brain of rats. Methods: Adult male SD rats were given by gavage once a day with 4ml/kg of drinking alcohol for 30 days as the model group, or normal saline with the same volume as the control group, or simultaneous intra gastric treatment, and intra gastric treatment with Melatonin (40ug/day) as treatment group. Memory and cognition were access by Morris Water Maze after the final intra gastric. After sacrifice, western blot and ELISA were carried out to check multiple protein levels and activities related to oxidative stress AD pathology. Results: Long-term drinking leads to a decrease of PP2A activity, an increase of GSK-3b activity, a decrease of SOD activity, an increase of MDA level, and abnormal hyperphosphorylation of tau at serine 199, serine 396 and serine 404 in both hippocampus and cortex. Morris water maze behavioral test revealed that alcohol treated rats induced spatial reference memory and memory consolidation deficits. Treatment of melatonin, an inhibitor of oxidative stress, attenuates the decrease of PP2A activity, increase of GSK-3b activity, decrease of SOD activity, increase of MDA level and tau hyperphosphorylation. Conclusions: These findings suggest that longterm drinking induced oxidative stress leads to GSK-3b activation, PP2A inhibition, and then tau hyperphosphorylation and cognitive deficit. Melatonin, an inhibitor of oxidative stress, attenuated these changes to some extent. Our study provided a clear insight, for the treatment of AD and other oxidative stress related pathology.