Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Thursday, January 12, 2017

Parahippocampal Cortex Mediates the Relationship between Lutein and Crystallized Intelligence in Healthy, Older Adults

What ever the hell crystallized intelligence is. Probably doesn't apply to us, we are not healthy. But ask your doctor anyway.
http://journal.frontiersin.org/article/10.3389/fnagi.2016.00297/full
Marta K. Zamroziewicz1,2,3, Erick J. Paul1,2, Chris E. Zwilling1,2, Elizabeth J. Johnson4, Matthew J. Kuchan5, Neal J. Cohen2,3,6,7 and Aron K. Barbey1,2,3,6,7,8,9,10*
  • 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:
  1. spinach,
  2. kale,
  3. broccoli,
  4. cabbage,
  5. yellow carrots,
  6. mango,
  7. orange,
  8. papaya,
  9. red or green pepper
  10. and also in egg yolks and animal fats since animals consume this pigment from plants.
More at link.

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