Nutrition for the ageing brain: towards evidence for an optimal diet

As people age they become increasingly susceptible to chronic and extremely debilitating brain diseases. The precise cause of the neuronal degeneration underlying these disorders, and indeed normal brain ageing remains however elusive. Considering the limits of existing preventive methods, there is a desire to develop effective and safe strategies. Growing preclinical and clinical research in healthy individuals or at the early stage of cognitive decline has demonstrated the beneficial impact of nutrition on cognitive functions. The present review is the most recent in a series produced by the Nutrition and Mental Performance Task Force under the auspice of the International Life Sciences Institute Europe (ILSI Europe). The latest scientific advances specific to how dietary nutrients and non-nutrient may affect cognitive ageing are presented. Furthermore, several key points related to mechanisms contributing to brain ageing, pathological conditions affecting brain function, and brain biomarkers are also discussed. Overall, findings are inconsistent and fragmented and more research is warranted to determine the underlying mechanisms and to establish dose-response relationships for optimal brain maintenance in different population subgroups. Such approaches are likely to provide the necessary evidence to develop research portfolios that will inform about new dietary recommendations on how to prevent cognitive decline

Chronic administration of 2’-FL potentiates the acquisition of an operant conditioning task in behaving rats, but this positive effect was prevented by a bilateral vagotomy.

<p>(A,B) Four (Control-Sham, white bar and circles; Control-Vagotomized, grey bar and circles; 2’-FL-Sham, red bar and circles; and, 2’-FL-Vagotomized, black bar and circles) groups of rats (n = 10 per group) were trained to press a lever to obtain a food pellet using a fixed-ratio (1:1) schedule. In this situation, animals have to press the lever just one time to obtain a pellet of food. A tone provided by a loudspeaker indicated the beginning and end of the session. Each session lasted for 20 min. (C) Time to reach criterion (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0166070#sec002" target="_blank">Methods</a>) for the four experimental groups in the fixed-ratio (1:1) schedule. Although no significant differences were reached between groups, the 2’-FL-Sham group presented a tendency to acquire the task faster than the 2’-FL-Vagotomized (<i>P</i> = 0.053) and the Control-Vagotomized (<i>P</i> = 0.053) groups. (D) Daily performance in the Skinner box of animals included in the four groups during the fixed-ratio (1:1) schedule. Significant differences were observed between the 2’-FL-Sham group and the 2’-FL-Vagotomized (■, <i>P</i> ≤ 0.05) and the Control-Vagotomized (*, <i>P</i> < 0.05) groups.</p

The chronic administration of 2’-FL potentiated LTP evoked at the hippocampal CA3-CA1 synapse in behaving rats, but this positive effect was prevented by a bilateral vagotomy.

<p>(A) The diagram illustrated how rats were prepared for the chronic recording of fEPSPs evoked at the hippocampal CA3-CA1 synapse. Bipolar stimulation electrodes were implanted on Schaffer collaterals, while a recording tetrode was aimed at ipsilateral stratum radiatum underneath the CA1 area. (B) A LTP test was carried out in three groups of animals (Control group, black circles; Fucose group, white circles; and 2’-FL group, red circles). After 15 min of baseline records (Day 1) animals were stimulated with a HFS protocol (vertical dotted line). Recording was carried out for 30 min after the HFS protocol. Additional recordings were carried out for 15 min during two additional days (Days 2 and 3). Illustrated data were collected from n ≥ 20 electrodes/group implanted in n ≥ 5 animals/group. Note that the 2'-FL group presented significantly (*, <i>P</i> ≤ 0.05) larger LTP values than the other two groups. (C) An additional LTP test was carried out for four groups of animals (Control-Sham group, white circles; Control-Vagotomized group, grey circles; 2’-FL-Sham group, red circles; and, 2’-FL-Vagotomized group, black circles). Animals were stimulated for two successive days with the same HFS protocol. Recording was carried out for 30 min after the two HFS (vertical dotted lines) protocols (Days 1 and 2). Additional recordings were carried out for 15 min during three additional days (Days 3–5). Illustrated data were collected from n ≥ 20 electrodes/group implanted in n ≥ 7 animals/group. Note that the 2'-FL-Sham group presented significantly larger LTP values than the Control-Sham (▲, <i>P</i> ≤ 0.05), Control-VG (#, <i>P</i> ≤ 0.05), and 2’-FL-VG (*, <i>P</i> ≤ 0.05) groups at the indicated recording times. In addition, the control-Sham group presented larger LTP values than the Control-VG (●, <i>P</i> ≤ 0.05), and the 2’-FL-VG ($, <i>P</i> ≤ 0.05) groups. Finally, the 2’-FL-VG group presented larger LTP values than the Control-VG (■, <i>P</i> ≤ 0.05) group for the 2nd recording day, although this situation was reversed during the 4th recording day.</p