n3 fatty acid deficiency accelerated the impairment of mouse brain function induced by stored amyloid beta protein
n3 fatty acid deficiency accelerated the impairment of mouse brain function induced by stored amyloid beta protein
Year: 2014
Authors: Iwanaga, S.
Publication Name: ISSFAL International Congress, Stockholm, Sweden June 28 – July 1
Publication Details: ID# Sunday S10.01
Abstract:
Several studies have reported that the administration of n3 polyunsaturated fatty acid (n3 PUFA), especially docosahexaenoic acid (DHA) reduced risk of Alzheimer's disease (AD). In this study, we observed the sensitivity of βamyloid protein (A beta ) effects in the DHA deficient mouse brain. Mice were fed either an n3 fatty acid deficient (n3 Def) or adequate (n3 Adq) diet for two generations. The content of PUFAs in the n3 Def diet was 16 percent linoleic acid
(LA), 0.15 percent alpha linolenic acid (ALA) whereas PUFAs in the n3 Adq diet contained
15.5 percent LA and 3.0 percent ALA. Half of the mice in each diet group were administered
3 nmol aggregated A beta (2535) intracerebroventricularly when they were 6 weeks of age. After 3 weeks, mice were evaluated with respect to their learning ability using the Morris water maze test. After the behavioral experiment, the fatty acid composition in their hippocampus and the amount of lipid peroxide in striatum were measured. In the water maze, the escape latency, which is the time required to reach the hidden platform, in the A beta treated n3 Adq mice was similar to that of the sham operated n3 Adq mice. On the other hand, n3 Def mice exhibited significantly poorer learning ability after A beta injection. Also the increase in lipid peroxide in the n3 Def group was greater than that of the n3 Adq group. There were no significant differences in the hippocampal DHA content between A beta injection and sham groups within each diet group, although that of n 3 Adq group was markedly higher than that of n3 Def group. These results suggested that the deficiency of brain DHA increased the damaging effects of amyloid beta protein in the brain and that dietary n3 fatty acid is protective against this impairment of learning ability. (Authors abstract)
(LA), 0.15 percent alpha linolenic acid (ALA) whereas PUFAs in the n3 Adq diet contained
15.5 percent LA and 3.0 percent ALA. Half of the mice in each diet group were administered
3 nmol aggregated A beta (2535) intracerebroventricularly when they were 6 weeks of age. After 3 weeks, mice were evaluated with respect to their learning ability using the Morris water maze test. After the behavioral experiment, the fatty acid composition in their hippocampus and the amount of lipid peroxide in striatum were measured. In the water maze, the escape latency, which is the time required to reach the hidden platform, in the A beta treated n3 Adq mice was similar to that of the sham operated n3 Adq mice. On the other hand, n3 Def mice exhibited significantly poorer learning ability after A beta injection. Also the increase in lipid peroxide in the n3 Def group was greater than that of the n3 Adq group. There were no significant differences in the hippocampal DHA content between A beta injection and sham groups within each diet group, although that of n 3 Adq group was markedly higher than that of n3 Def group. These results suggested that the deficiency of brain DHA increased the damaging effects of amyloid beta protein in the brain and that dietary n3 fatty acid is protective against this impairment of learning ability. (Authors abstract)
