Docosahexaenoic acid (C22:6, n-3), a major n-3 fatty acid of the brain, has been implicated in restoration and enhancement of memory-related functions. Because Alzheimer's disease impairs memory, and infusion of amyloid-b (Ab) peptide (1-40) into the rat cerebral ventricle reduces learning ability, we investigated the effect of dietary pre-administration of docosahexaenoic acid on avoidance learning ability in Ab peptide-produced Alzheimer's disease model rats. After a mini-osmotic pump filled with Ab peptide or vehicle was implanted in docosahexaenoic acid-fed and control rats, they were subjected to an active avoidance task in a shuttle avoidance system apparatus. Pre-administration of docosahexaenoic acid had a profoundly beneficial effect on the decline in avoidance learning ability in the Alzheimer's disease model rats, associated with an increase in the cortico-hippocampal docosahexaenoic acid/arachidonic acid molar ratio, and a decrease in neuronal apoptotic products. Docosahexaenoic acid pre-administration furthermore increased cortico-hippocampal reduced glutathione levels and glutathione reductase activity, and suppressed the increase in lipid peroxide and reactive oxygen species levels in the cerebral cortex and hippocampus of the Alzheimer's disease model rats, suggesting an increase in antioxidative defence. Docosahexaenoic acid is thus a possible prophylactic means for preventing the learning deficiencies of Alzheimer's disease.

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We investigated whether administration of docosahexaenoic acid (DHA), a major (n-3) fatty acid of the brain, ameliorates the impairment of learning ability in an animal model of Alzheimer's disease (AD), rats infused with amyloid-beta (Abeta) peptide (1-40) into the cerebral ventricle. Inbred 3rd generation male rats (20 wk old) fed a fish oil-deficient diet were randomly divided into 4 groups: a vehicle group, an Abeta peptide-infused group (Abeta group), a DHA group, and an Abeta + DHA group. A mini-osmotic pump filled with Abeta peptide or vehicle was implanted in the rats, and they were tested for learning ability-related reference and working memory in an 8-arm radial maze. The rats were then orally fed DHA dissolved in 5% gum Arabic solution at 300 mg/(kg . d) (DHA and Abeta + DHA groups) or vehicle alone (vehicle and Abeta groups) and tested again for learning ability. DHA administered for 12 wk significantly reduced the increase in the number of reference and working memory errors in the Abeta-infused rats, and increased both the cortico-hippocampal level of DHA and the molar ratio of DHA/arachidonic acid, suggesting an amelioration of the impaired spatial cognition learning ability. Furthermore, DHA suppressed the increases in the levels of lipid peroxide and reactive oxygen species in the cerebral cortex and the hippocampus of Abeta-infused rats, suggesting that DHA increases antioxidative defenses. DHA is thus a possible therapeutic agent for ameliorating learning deficiencies due to Alzheimer's disease.

Technidilaton (TD) was proposed long ago in the technicolor near criticality/conformality. To reveal the critical behavior of TD, we explicitly compute the nonperturbative contributions to the scale anomaly h i and to the technigluon condensate hG 2 i, which are generated by the dynamical mass m of the technifermions. Our computation is based on the (improved) ladder Schwinger-Dyson equation, with the gauge coupling replaced by the two-loop running coupling ðÞ having the Caswell-BanksZaks infrared fixed point à : ðÞ ' ¼ à for the infrared region m < < à TC , where à TC is the intrinsic scale (analogue of à QCD of QCD) relevant to the perturbative scale anomaly. We find that Àh i=m 4 ! const Þ 0 and hG 2 i=m 4 ! ð= cr À 1Þ À3=2 ! 1 in the criticality limit m=à TC $ expðÀ=ð= cr À 1Þ 1=2 Þ ! 0 ( ¼ à & cr , or N f % N cr f ) (''conformal edge''). Our result precisely reproduces the formal identity h i ¼ ððÞ=4 2 ÞhG 2 i, where ðÞ ¼ à TC @ @à TC ¼ Àð2 cr =Þ Á ð= cr À 1Þ 3=2 is the nonperturbative beta function corresponding to the above essential singularity scaling of m=à TC . Accordingly, the partially conserved dilatation current implies ðM TD =mÞ 2 ðF TD =mÞ 2 ¼ À4h i=m 4 ! const Þ 0 at criticality limit, where M TD is the mass of TD and F TD the decay constant of TD. We thus conclude that at criticality limit the TD could become a ''true (massless) Nambu-Goldstone boson'' M TD =m ! 0, only when m=F TD ! 0, namely, getting decoupled, as was the case of ''holographic technidilaton'' of Haba-Matsuzaki-Yamawaki. The decoupled TD can be a candidate of dark matter.