http://journal.frontiersin.org/article/10.3389/fnagi.2016.00297/full
- 1Decision Neuroscience Laboratory, University of Illinois Urbana-Champaign, Urbana, IL, USA
- 2Beckman Institute for Advanced Science and Technology, University of Illinois Urbana-Champaign, Urbana, IL, USA
- 3Neuroscience Program, University of Illinois Urbana-Champaign, Urbana, IL, USA
- 4Jean Mayer USDA Human Nutrition Center on Aging, Tufts University, Boston, MA USA
- 5Research, Scientific and Medical Affairs, Abbott Nutrition, Columbus, OH, USA
- 6Department of Psychology, University of Illinois Urbana-Champaign, Urbana, IL, USA
- 7Carle Neuroscience Institute, Carle Foundation Hospital, Urbana, IL, USA
- 8Department of Internal Medicine, University of Illinois Urbana-Champaign, Urbana, IL, USA
- 9Department of Speech and Hearing Science, University of Illinois Urbana-Champaign, Urbana, IL, USA
- 10Institute for Genomic Biology, University of Illinois Urbana-Champaign, Champaign, IL, USA
Introduction: Although, diet has a
substantial influence on the aging brain, the relationship between
dietary nutrients and aspects of brain health remains unclear. This
study examines the neural mechanisms that mediate the relationship
between a carotenoid important for brain health across the lifespan,
lutein, and crystallized intelligence in cognitively intact older
adults. We hypothesized that higher serum levels of lutein are
associated with better performance on a task of crystallized
intelligence, and that this relationship is mediated by gray matter
structure of regions within the temporal cortex. This investigation aims
to contribute to a growing line of evidence, which suggests that
particular nutrients may slow or prevent aspects of cognitive decline by
targeting specific features of brain aging.
Methods: We examined 76 cognitively
intact adults between the ages of 65 and 75 to investigate the
relationship between serum lutein, tests of crystallized intelligence
(measured by the Wechsler Abbreviated Scale of Intelligence), and gray
matter volume of regions within the temporal cortex. A three-step
mediation analysis was implemented using multivariate linear regressions
to control for age, sex, education, income, depression status, and body
mass index.
Results: The mediation analysis
revealed that gray matter thickness of one region within the temporal
cortex, the right parahippocampal cortex (Brodmann's Area 34), partially
mediates the relationship between serum lutein and crystallized
intelligence.
Conclusion: These results suggest that
the parahippocampal cortex acts as a mediator of the relationship
between serum lutein and crystallized intelligence in cognitively intact
older adults. Prior findings substantiate the individual relationships
reported within the mediation, specifically the links between (i) serum
lutein and temporal cortex structure, (ii) serum lutein and crystallized
intelligence, and (iii) parahippocampal cortex structure and
crystallized intelligence. This report demonstrates a novel structural
mediation between lutein status and crystallized intelligence, and
therefore provides further evidence that specific nutrients may slow or
prevent features of cognitive decline by hindering particular aspects of
brain aging. Future work should examine the potential mechanisms
underlying this mediation, including the antioxidant, anti-inflammatory,
and membrane modulating properties of lutein.
Introduction
As the older adult population expands, the economic
burden of care and treatment of age-related health disorders also rises.
Between 2015 and 2060, the United States will experience significant
growth of its older population, with the size of the population aged 65
and over more than doubling from an estimated 46 million in 2015 to 98
million in 2060 (Mather et al., 2015).
Therefore, successful strategies to promote healthy brain aging are of
significant interest to public health initiatives in the United States.
Nutrition is a promising target for intervention efforts to support healthy brain aging (Zamroziewicz and Barbey, 2016).
Accumulating evidence indicates that particular nutrients may slow or
prevent aspects of age-related cognitive decline by targeting specific
features of brain aging. Studies that couple neuroimaging techniques
with neuropsychological testing provide insight into mechanisms of
action through which particular nutrients might influence specific
aspects of age-related cognitive decline (Bowman et al., 2012; Zamroziewicz et al., 2015; Boespflug et al., 2016; Gu et al., 2016).
While some nutrients may be effective at preventing late-life changes
in the brain, other nutritional factors may accumulate across the
lifespan and therefore confer neuroprotection in the aging brain (Söderberg et al., 1990; Coyle and Puttfarcken, 1993).
Identifying the mechanisms through which nutrients provide
neuroprotective effects will help guide the development of successful
lifelong dietary strategies for healthy brain aging.
Carotenoids are naturally occurring pigments made by plants, and can only be acquired through the diet (Erdman et al., 2015).
Xanthophylls are a subclass of carotenoids, which have a polar
molecular structure and therefore possess unique membrane-spanning
properties (Erdman et al., 2015; Widomska et al., 2016).
As compared to the other dietary carotenoids, xanthophylls
preferentially accumulate in neural tissue, with lutein accounting for
the majority of carotenoid accumulation in the brain (Craft et al., 2004; Johnson, 2012; Johnson et al., 2013; Li et al., 2014; Vishwanathan et al., 2014b; Widomska et al., 2016).
As the most prevalent carotenoid in the brain, lutein is thought
provide a variety of neuroprotective benefits. Candidate mechanisms of
action are primarily based on the unique membrane spanning properties of
lutein and include influencing membrane properties, such as fluidity,
interneuronal communication via gap junctions, ion exchange, oxygen
diffusion, membrane stability, and preventing oxidation and inflammation
(Stahl and Sies, 1996, 2001; Paiva and Russell, 1999; Krinsky, 2002; Izumi-Nagai et al., 2007; Johnson, 2014; Widomska and Subczynski, 2014; Erdman et al., 2015). Lutein accretes in the brain across the entire lifespan, and may therefore contribute to brain health in a lifelong manner (Renzi et al., 2014; Bovier and Hammond, 2015; Lieblein-Boff et al., 2015).
Notably, lutein is selectively distributed in gray matter, and has been
detected in the prefrontal cortex, the temporal cortex, and the
hippocampus (Craft et al., 2004; Vishwanathan et al., 2014b).
Blood levels of lutein correlate with brain concentrations of lutein in
older adults, suggesting that blood concentrations can serve a measure
of lutein status in the brain (Johnson et al., 2013).
Lutein status has been linked to cognitive performance across the lifespan (Feeney et al., 2013; Johnson et al., 2013; Renzi et al., 2014; Vishwanathan et al., 2014a; Bovier and Hammond, 2015). Of particular interest, lutein levels have been linked to memory and general intelligence (Feeney et al., 2013; Johnson et al., 2013; Vishwanathan et al., 2014a),
which are cognitive constructs closely related to crystallized
intelligence. Crystallized intelligence refers to the ability to
retrieve and use information that has been acquired throughout life (Horn and Cattell, 1966).
Although most aspects of cognitive function undergo age-related
decline, certain aspects of cognition—like crystallized intelligence—are
spared and even show improvement with age (Craik and Bialystok, 2006; Park and Reuter-Lorenz, 2009).
Measuring crystallized intelligence may therefore be a way to assess
the lifelong impact of nutritional factors, rather than the immediate
effects of nutrients on preventing age-related decline (Craik and Bialystok, 2006).
Crystallized intelligence is dependent upon the temporal
cortex, and particular regions of the temporal cortex may play key
roles in implementing this cognitive function (Colom et al., 2009; Barbey et al., 2012).
In general, structural integrity of the temporal cortex is associated
with performance on tasks of crystallized intelligence, but integrity of
specific regions within the temporal cortex may underlie the
preservation of this cognitive function in aging (Choi et al., 2008). For example, the parahippocampal cortex plays a role in mediating the storage of knowledge about objects (Ricci et al., 1999; Aminoff et al., 2013).
This region of the temporal cortex shows resistance to age-related
structural decline in the absence of neurodegenerative disease, unlike
other regions within the temporal cortex that show significant cortical
thinning even in healthy aging (Salat et al., 2004; Jiang et al., 2014).
Although the sparing of particular regions within the temporal cortex
may be linked to the preservation of crystallized intelligence in
healthy aging, the question remains: do particular neuroprotective
nutrients like lutein underlie this sparing of cognition and brain
health?
In summary, increasing evidence suggests that lutein may
be a reliable nutrient biomarker for healthy brain aging: (i) among the
carotenoids, lutein accounts for the majority of accumulation in the
brain and provides unique neuroprotective benefits, (ii) lutein status
has been linked to cognitive performance across the lifespan, and (iii)
lutein is selectively distributed in gray matter of brain regions known
to underlie the preservation of cognitive function in healthy brain
aging. However, the core brain structures upon which lutein may act to
preserve cognition have not been investigated. Prior research suggests
that lutein plays a neuroprotective role across the lifespan,
crystallized intelligence is resistant to age-related decline, and
specific regions of the temporal cortex may underlie the preservation of
crystallized intelligence. This study aims to explore the role of
structures within the temporal cortex in mediating the relationship
between serum lutein levels and crystallized intelligence in healthy
older adults.
From another site:
Lutein can be extracted from marigold flower and is present in:
Lutein can be extracted from marigold flower and is present in:
- spinach,
- kale,
- broccoli,
- cabbage,
- yellow carrots,
- mango,
- orange,
- papaya,
- red or green pepper
- and also in egg yolks and animal fats since animals consume this pigment from plants.
More at link.
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