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

Mean (SD) cognitive domain scores in patients and in the normative data set.

<p>Mean (SD) cognitive domain scores in patients and in the normative data set.</p

Work-related questions.

<p>Work-related questions.</p

Correlations between confounding variables and HRQoL, and working hours.

<p>Max., maximum;</p><p>*P<0.005;</p><p>**P<0.05.</p

Correlations between cognitive scores and working hours.

<p>Max., maximum; *, P<0.04; all other P values >0.125.</p

CONSORT chart showing flow of participants through the trial.

<p>Assessment of POCD required completion of seven cognitive assessments which were not all completed for all individuals at all timepoints. Presence/absence of POCD was therefore determined as follows throughout the trial. Week 1: Intervention group – 19, Control group – 28; Week 12: Intervention group – 24; Control group – 33; Week 52: Intervention group 27; Control group – 32.</p

Outcome Comparisons: Cognitive Outcomes (Change from Baseline between groups).

<p>Results presented as both median with upper and lower quartiles and mean with Standard Deviation.</p><p>MWU – Mann-Whitney U test, SD – Standard Deviation, IQR – Inter Quartile Range.</p>*<p>Statistically significant (p<0·05).</p

RCT Outcome Comparisons: Post-Operative Cognitive Decline (POCD).

<p>POCD at 1 week (n = 19 intervention group, n = 28 control group). POCD at 12 weeks (n = 24 intervention group, n = 33 control group). POCD at 52 weeks (n = 27 intervention group, n = 32 control group).</p

Baseline Sample Characteristics for the RCT.

<p>Baseline Sample Characteristics for the RCT.</p