DHA diet reduces AD pathology in young APPswe/PS1 Delta E9 transgenic mice: possible gender effects.
Epidemiological and clinical trial findings suggest that consumption of docosahexaenoic acid (DHA) lowers the risk of Alzheimer's disease (AD). We examined the effects of short-term (3 months) DHA enriched diet on plaque deposition and synaptic defects in forebrain of young APPswe/PS1 Delta E9 transgenic (tg) and non-transgenic (ntg) mice. Gas chromatography revealed a significant increase in DHA concomitant with a decrease of arachidonic acid in both brain and liver in mice fed with DHA. Female tg mice consumed relatively more food daily than ntg female mice, independent of diet. Plaque load was significantly reduced in the cortex, ventral hippocampus and striatum of female APPswe/PS1 Delta E9 tg mice on DHA diet compared to female tg mice on control diet. Immunoblot quantitation of the APOE receptor, LR11, which is involved in APP trafficking and A beta production, were unchanged in mice on DHA or control diets. Moreover drebrin levels were significantly increased in the hippocampus of tg mice on the DHA diet. Finally, in vitro DHA treatment prevented amyloid toxicity in cell cultures. Our findings support the concept that increased DHA consumption may play and important role in reducing brain insults in female AD patients.
Perez
Sylvia E
SE
Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612, USA.
Berg
Brian M
BM
Moore
Kenneth A
KA
He
Bin
B
Counts
Scott E
SE
Fritz
Jason J
JJ
Hu
Yuan-Shih
YS
Lazarov
Orly
O
Lah
James J
JJ
Mufson
Elliott J
EJ
D000544:Alzheimer Disease / Q000178:diet therapy* / Q000378:metabolism* / Q000503:physiopathology; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D001057:Apolipoproteins E / Q000378:metabolism; D016718:Arachidonic Acid / Q000378:metabolism; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D001923:Brain Chemistry / Q000502:physiology; D004195:Disease Models, Animal; D004281:Docosahexaenoic Acids / Q000378:metabolism* / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D006801:Humans; D008099:Liver / Q000378:metabolism; D026901:Membrane Transport Proteins / Q000378:metabolism; D051379:Mice; D008822:Mice, Transgenic; D009479:Neuropeptides / Q000378:metabolism; D058225:Plaque, Amyloid / Q000378:metabolism / Q000473:pathology; D053764:Presenilin-1 / Q000235:genetics; D016548:Prosencephalon / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D011973:Receptors, LDL / Q000378:metabolism; D012727:Sex Characteristics; D016896:Treatment Outcome
D016564:Amyloid beta-Protein Precursor; D001057:Apolipoproteins E; D026901:Membrane Transport Proteins; D009479:Neuropeptides; D053764:Presenilin-1; D011973:Receptors, LDL; C491168:Sorl1 protein, mouse; C053386:drebrins; D004281:Docosahexaenoic Acids; D016718:Arachidonic Acid