Groups of young (3-4 m) and aged (20–22 m) rats treated with EPA and DHA for 56 d
Deficits in LTP are reversed in the aged rats that received EPA or DPA
Deficits in spatial learning are reversed in the aged rats that received EPA or DPA
Preservation of cognitive function following n-3 PUFA supplementation in aged animals is supported by complementary anti-inflammatory, antioxidative, and metabolic effects
Short-term (6 w) and long-term (12 w) curcumin-supplemented diet to old rats (15 m)
12 w intervention ↑neurogenesis; 12 w treatment markedly upregulated genes implicated in synaptic transmission and memory formation, for example, Cav1 gene—implicated in both cholesterol metabolism in AD and synaptic plasticity
Only 12 w treatment ↑spatial memory
Beneficial effects, explained by the enhancing of adult neurogenesis and synaptic plasticity, may require an accumulated effect of the active metabolites over a prolonged period
Grape-derived polyphenolic preparation comprising a mixture of PAC
5 m treatment starting at 7 m of age (before AD neuropathology/cognitive deficits). 10 d treatment to assess pharmacokinetics and bioavailability. Tg2576 mice aged 22–24 m used to assess the effect of PAC metabolites on LTP
↑levels of metabolites from PAC monomers were detected in the plasma and brain of mice. Biosynthetic PAC monomer metabolite ↑LTP in the CA1 region and ↑phosphorylation of CREB at Ser133
Only the monomeric PAC improved spatial memory retention
Brain-targeted metabolite derived from a polyphenol is capable of restoring synaptic plasticity in the AD-afflicted hippocampal formation
Embryonic 14–16 d cortico-hippocampal neuronal cultures derived from Tg2576 AD mice
Cabernet Sauvignon (red wine derived poylphenol)
Cells were treated with varying doses of the polyphenols equivalent to moderate daily wine consumption in humans
Caberent Sauvignon brain-targeted metabolite quercetin-3-0-glucuronide reverses AD-type deficits in hippocampal basal synaptic transmission and LTP, via activation of cellular modulators of CREB protein signalling pathways.
N/A
Quercetin-3-O-glucuronide in the brain may simultaneously modulate multiple independent AD disease-modifying mechanisms, including enhancing synaptic plasticity
Multinutriet diet Fortasyn (FC), containing DHA, EPA, phospholipids, uridine monophosphate (UMP), choline, B vitamins, and antioxidants
At 2 months of age, the mice were put on either control or FC diet for the remainder of the experiment. Behavioral testing was performed at 9 m. MR imaging was performed at 11 m
No change in the levels of synaptophysin and neurogenesis MRS revealed decreased levels of glutamate in both the apoE knockout and wild-type mice increase in CBV in a region of mid-brain in the apoE ko and wild-type mice fed
Anxiolytic effect on apoE ko and wild-type mice. Improved learning and spatial memory performance only in the apoE knockout mice
n-3 PUFAs seem to exert their beneficial effects by improving synaptic function rather than by increasing synaptogenesis. Increase in CBV possibly reflects improvement in brain perfusion
Diet enriched with DHA, EPA, and UMP (DEU diet) or diet enriched with DHA, EPA, UMP as well as phospholipids, choline, folic acid, vitamins B6, B12, C, E, and selenium (FC diet)
Feeding the diets started when the mice reached the age of 2 months and was maintained for the remainder of the experiment. Animals underwent behavioral testing at 11 months of age and subsequently MRS measurements at 12 months of age
Both diets had no effect on reversing declines in the levels of N-acetylaspartylglutamate (tNAA) FC but not the DEU diet had a significantly higher amount of doublecortin positive cells FC diet ↓hippocampal levels of unbound choline-containing compounds in wild-type and transgenic animals
FC diet exerts an anxiolytic response Both DEU and FC diets had no effect on attenuating spatial learning or memory deficits
The FC diet was more effective than the DEU diet in counteracting neurodegenerative aspects of AD and enhancing processes involved in neuronal maintenance and repair. Specific multinutrient diets can influence AD pathophysiology, including enhancing brain plasticity.
