Jane M. Bell

TL;DR: This single-generational n-3 PUFA-deprived rat model, which demonstrated significant changes in brain lipid composition and in test scores for depression and aggression, may be useful for elucidating the contribution of disturbed brain PUFA metabolism to human depression, aggression, and bipolar disorder.

TL;DR: Equations derived from kinetic modeling demonstrated that unesterified unlabeled α‐LNA rapidly enters brain from plasma, but that its incorporation into brain phospholipid and triglyceride, as in the form of synthesized DHA, is ≤ 0.2% of the amount that enters the brain.

TL;DR: Mechanisms must exist in the adult rat brain to minimize DHA metabolic loss, and to do so even more effectively in the face of reduced n‐3 PUFA availability for only 15 weeks.

TL;DR: In rats fed even a diet containing low amounts of AA, the LA that enters brain is largely beta-oxidized, and is not a major source of AA in brain.

TL;DR: The brain's ability to synthesize DHA from alpha-LNA is very low and is not altered by n-3 PUFA deprivation, and because the liver's reported ability is much higher, and can be upregulated by the deficient diet, DHA converted by the liver from circulating alphaL NA is the source of the brain's DHA when DHA is not in the diet.