This study investigated the relationship between plasma phosphatidylcholine levels, cognitive flexibility, and prefrontal cortex thickness in older adults. The results showed that higher phosphatidylcholine levels were associated with better cognitive flexibility and greater prefrontal cortex thickness. Statistical analysis revealed that prefrontal cortex thickness mediated the relationship between phosphatidylcholine levels and cognitive performance. This suggests that phosphatidylcholine may help preserve cognitive flexibility in aging by maintaining the structural integrity of the prefrontal cortex.
Islamic Perspective on Nutrigenomic intervention in Postmenopausal Osteoporos...Hafizah R
Nutrigenomics is the study of the effects of foods and food constituents on gene expression. It is about how our DNA is transcribed into mRNA and then to proteins and provides a basis for understanding the biological activity of food components. The boundary between health and disease is often defined by a complex equilibrium between two elements, genetics and lifestyle.
The aim of nutrigenomics is to personalize nutrition and its effects on health by tailoring food to the individual genotype. The purpose of this review is to present the interaction between a genetic polymorphisms disorder which is Post-Menopausal Osteoporosis (PMO) and diet. Poor nutrition can be risk factor for diseases. Common dietary chemicals can act on the human genome, either directly or indirectly to alter gene expression or gene structure. The degree to which diet influences the balance between health and disease depends on an individual‟s genetic makeup.
Islamic Perspective on Nutrigenomic intervention in Postmenopausal Osteoporos...Hafizah R
Nutrigenomics is the study of the effects of foods and food constituents on gene expression. It is about how our DNA is transcribed into mRNA and then to proteins and provides a basis for understanding the biological activity of food components. The boundary between health and disease is often defined by a complex equilibrium between two elements, genetics and lifestyle.
The aim of nutrigenomics is to personalize nutrition and its effects on health by tailoring food to the individual genotype. The purpose of this review is to present the interaction between a genetic polymorphisms disorder which is Post-Menopausal Osteoporosis (PMO) and diet. Poor nutrition can be risk factor for diseases. Common dietary chemicals can act on the human genome, either directly or indirectly to alter gene expression or gene structure. The degree to which diet influences the balance between health and disease depends on an individual‟s genetic makeup.
Exercise is any bodily activity that enhances or maintain physical fitness and overall health, Exercise with its Countless Benefits is the logical salvage for a group of diseases related to inactivity . In view of the prevalence, global reach and health effect of these physical inactivity related diseases, the issue should be appropriately described as pandemic, with far-reaching health, economic, social and Environmental consequences.These diseases include, Obesity, Coronary artery disease, Diabetes, Hypertension, Cancer, Depression and anxiety, Arthritis, Osteoporosis, Etc, etc, etc… I think we have no option except doing regular exercises if we seriously searching for a salvage to escape the bad and serious consequences of these new life style diseases.
Osteogenesis Imperfecta is a genetic connective tissue disorder. It has clinically heterogeneous four types. Type 2 is the most severe and perinatally lethal form having small thorax, curved limbs and blue/gray sclerae. It is further subclassified into 3 types. A baby with sign and symptoms with macrocephaly, retrognathia, low set ears, widely placed eyes with white sclerae, complete cleft palate, narrow chest, curved and shortened limbs, B/L CTEV, left undescended testis with hypospadiasis was reported. This rare case was thoroghly examined and investigated which came out to a case of 'Osteogenesis Imperfecta type 2 A' having white sclerae. So case having such symptoms were should be investigated for Osteogenesis Imperfecta.
Review by Louis B. Cady, MD (Cady Wellness Institute) of need for vitamin and mineral supplements, current evidence for loss of minerals and nutrients in soils. Reasonable strategies for identifying supplement needs. Understand how declining nutrients, inadequate intake of recommended servings of fruits and vegetables all contribute to chronic health conditions.
Osteoarthritis is the most common disease of women after menopause. There are many factors to develop the disease. Hormones play important role to in this context. The objective of the present study is to determine whether the levels of thyroid and sex hormones are associated with osteoarthritis (OA) in postmenopausal women. Forty three patients suffering from OA and twenty control subjects were included in this study. Thyroid and sex hormones were measured in the serum by enzyme linked immunosorbent assay technique. In OA patients serum estrogen levels were low as compared to control subjects(p<0.001), but these patients did not show any significant change in thyroid hormones and progesterone hormone levels when compared with control subjects. The findings suggest that estrogen deficiency after menopause may contribute to develop OA in postmenopausal women.
Depression is an insidious issue in the US and elsewhere. Lifestyle habits that are very different from our ancestral environment may be to blame, and one particularly problematic area is food choice. Depressive symptoms share much in common with the adaptive features of sickness behavior, which is functional when operating in an environment of ancestrally normal immune stressor. Modern diets likely activate the immune system (primarily the inflammatory response) and induce the cascade of adaptive responses that collective make up sickness behavior. Due to their similarities, these may then diagnosed as depression. In this talk, I discuss the links among diet, depression, and inflammation, as well as highlighting some specific dietary components that contribute to this response.
Sleep is a crucial health issue - but it is often ignored by both individuals and the medical community. Sleep has been shown to substantially impact almost every major health condition including Diabetes, Cancer, Obesity, Heart Disease, and Mental Health. It's time for sleep to take it's rightful place in keeping us health. This presentation gives some of the cold, hard facts behind why sleep is such a silent killer.
971Received March 15, 2017Accepted for publication May 16,.docxsleeperharwell
971
Received March 15, 2017
Accepted for publication May 16, 2017
J Nutr Health Aging
Volume 21, Number 9, 2017
Introduction
Iodine is one of the three key micronutrient for which
deficiency is highlighted as a major public health issue by the
World Health Organisation, and the most preventable cause
of mental retardation and brain damage (1). While the role of
iodine in neurodevelopment has become better understood in
early life, there is little evidence available regarding the lifelong
impact of iodine on brain function. European countries are
usually assumed to have sufficient dietary iodine intake, but the
UK has been classified as insufficient (2, 3). This is a particular
threat to pregnant women and their offspring, since insufficient
early exposure to iodine leads to blunted mental capacity.
Indeed, the offspring of mothers taking part in the ALSPAC
study (www.bristol.ac.uk/alspac/) had lower IQ at age 8 if
maternal iodine in pregnancy had been in the lowest quartile
(4). Childhood IQ is known to be one of the key determinants
of later life cognition and wellbeing, and is associated with
mortality, morbidity and frailty in old age (5).
Iodine is obtained mainly through the diet, with no ongoing
iodine-fortification programme in the UK. The main sources
of iodine in the British diet are milk and dairy products,
as well as fish and seafood. While cross-sectional surveys
revealed mild insufficiency in the population (1), recent
studies have highlighted that most women struggle to reach the
recommended iodine daily intake (150 µg/day), a recommended
intake that increases during pregnancy to 250 µg/day (6).
Iodine deficiency, mainly in children and young adults, has
been suggested to cause certain brain proteins to be down-
regulated in particular brain regions, anterior commissure
axons and mRNA expression to be reduced, and dendrite size
to be altered resulting in potential premature cell apoptosis.
Additionally, iodine deficiency may cause a reduction in
cerebellar cell size and decreased myelination throughout the
central nervous system (7), and, therefore, may be related to
brain atrophy and brain white matter damage. Altogether, such
changes are likely to affect cognitive functions. Preservation
of mental / cognitive capacities is key in having a healthy long
DIETARY IODINE EXPOSURE AND BRAIN STRUCTURES AND COGNITION
IN OLDER PEOPLE. EXPLORATORY ANALYSIS
IN THE LOTHIAN BIRTH COHORT 1936
M. DEL C. VALDÉS HERNÁNDEZ1,2*, J. KYLE3, J. ALLAN4, M. ALLERHAND1, H. CLARK3,
S. MUÑOZ MANIEG1,2, N.A. ROYLE1,2, A.J. GOW1,5, A. PATTIE1,6, J. CORLEY1,6, M.E. BASTIN1,2,
J.M. STARR1, J.M. WARDLAW1,2, I.J. DEARY1,6, E. COMBET7*
1. Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK; 2. Department of Neuroimaging Sciences, Centre for Clinical Brain Sciences,
University of Edinburgh, Edinburgh, UK; 3. Department of Nutrition, University of Aberdeen, Aberdee.
“Cognition is a field of thought processes by which an individual processes information through skills of perception, thinking, memory, learning and attention”
Zinc, the 2nd most abundant trace micronutrient
Almost 40 to 50% vulnerable group are zinc deficient
Zinc deficiency effect cognition development by
Modulating zinc homeostasis
Neurogenesis
Strategies like diet diversification, fortification and supplementation are helpful in alleviating deficiency
Exercise is any bodily activity that enhances or maintain physical fitness and overall health, Exercise with its Countless Benefits is the logical salvage for a group of diseases related to inactivity . In view of the prevalence, global reach and health effect of these physical inactivity related diseases, the issue should be appropriately described as pandemic, with far-reaching health, economic, social and Environmental consequences.These diseases include, Obesity, Coronary artery disease, Diabetes, Hypertension, Cancer, Depression and anxiety, Arthritis, Osteoporosis, Etc, etc, etc… I think we have no option except doing regular exercises if we seriously searching for a salvage to escape the bad and serious consequences of these new life style diseases.
Osteogenesis Imperfecta is a genetic connective tissue disorder. It has clinically heterogeneous four types. Type 2 is the most severe and perinatally lethal form having small thorax, curved limbs and blue/gray sclerae. It is further subclassified into 3 types. A baby with sign and symptoms with macrocephaly, retrognathia, low set ears, widely placed eyes with white sclerae, complete cleft palate, narrow chest, curved and shortened limbs, B/L CTEV, left undescended testis with hypospadiasis was reported. This rare case was thoroghly examined and investigated which came out to a case of 'Osteogenesis Imperfecta type 2 A' having white sclerae. So case having such symptoms were should be investigated for Osteogenesis Imperfecta.
Review by Louis B. Cady, MD (Cady Wellness Institute) of need for vitamin and mineral supplements, current evidence for loss of minerals and nutrients in soils. Reasonable strategies for identifying supplement needs. Understand how declining nutrients, inadequate intake of recommended servings of fruits and vegetables all contribute to chronic health conditions.
Osteoarthritis is the most common disease of women after menopause. There are many factors to develop the disease. Hormones play important role to in this context. The objective of the present study is to determine whether the levels of thyroid and sex hormones are associated with osteoarthritis (OA) in postmenopausal women. Forty three patients suffering from OA and twenty control subjects were included in this study. Thyroid and sex hormones were measured in the serum by enzyme linked immunosorbent assay technique. In OA patients serum estrogen levels were low as compared to control subjects(p<0.001), but these patients did not show any significant change in thyroid hormones and progesterone hormone levels when compared with control subjects. The findings suggest that estrogen deficiency after menopause may contribute to develop OA in postmenopausal women.
Depression is an insidious issue in the US and elsewhere. Lifestyle habits that are very different from our ancestral environment may be to blame, and one particularly problematic area is food choice. Depressive symptoms share much in common with the adaptive features of sickness behavior, which is functional when operating in an environment of ancestrally normal immune stressor. Modern diets likely activate the immune system (primarily the inflammatory response) and induce the cascade of adaptive responses that collective make up sickness behavior. Due to their similarities, these may then diagnosed as depression. In this talk, I discuss the links among diet, depression, and inflammation, as well as highlighting some specific dietary components that contribute to this response.
Sleep is a crucial health issue - but it is often ignored by both individuals and the medical community. Sleep has been shown to substantially impact almost every major health condition including Diabetes, Cancer, Obesity, Heart Disease, and Mental Health. It's time for sleep to take it's rightful place in keeping us health. This presentation gives some of the cold, hard facts behind why sleep is such a silent killer.
971Received March 15, 2017Accepted for publication May 16,.docxsleeperharwell
971
Received March 15, 2017
Accepted for publication May 16, 2017
J Nutr Health Aging
Volume 21, Number 9, 2017
Introduction
Iodine is one of the three key micronutrient for which
deficiency is highlighted as a major public health issue by the
World Health Organisation, and the most preventable cause
of mental retardation and brain damage (1). While the role of
iodine in neurodevelopment has become better understood in
early life, there is little evidence available regarding the lifelong
impact of iodine on brain function. European countries are
usually assumed to have sufficient dietary iodine intake, but the
UK has been classified as insufficient (2, 3). This is a particular
threat to pregnant women and their offspring, since insufficient
early exposure to iodine leads to blunted mental capacity.
Indeed, the offspring of mothers taking part in the ALSPAC
study (www.bristol.ac.uk/alspac/) had lower IQ at age 8 if
maternal iodine in pregnancy had been in the lowest quartile
(4). Childhood IQ is known to be one of the key determinants
of later life cognition and wellbeing, and is associated with
mortality, morbidity and frailty in old age (5).
Iodine is obtained mainly through the diet, with no ongoing
iodine-fortification programme in the UK. The main sources
of iodine in the British diet are milk and dairy products,
as well as fish and seafood. While cross-sectional surveys
revealed mild insufficiency in the population (1), recent
studies have highlighted that most women struggle to reach the
recommended iodine daily intake (150 µg/day), a recommended
intake that increases during pregnancy to 250 µg/day (6).
Iodine deficiency, mainly in children and young adults, has
been suggested to cause certain brain proteins to be down-
regulated in particular brain regions, anterior commissure
axons and mRNA expression to be reduced, and dendrite size
to be altered resulting in potential premature cell apoptosis.
Additionally, iodine deficiency may cause a reduction in
cerebellar cell size and decreased myelination throughout the
central nervous system (7), and, therefore, may be related to
brain atrophy and brain white matter damage. Altogether, such
changes are likely to affect cognitive functions. Preservation
of mental / cognitive capacities is key in having a healthy long
DIETARY IODINE EXPOSURE AND BRAIN STRUCTURES AND COGNITION
IN OLDER PEOPLE. EXPLORATORY ANALYSIS
IN THE LOTHIAN BIRTH COHORT 1936
M. DEL C. VALDÉS HERNÁNDEZ1,2*, J. KYLE3, J. ALLAN4, M. ALLERHAND1, H. CLARK3,
S. MUÑOZ MANIEG1,2, N.A. ROYLE1,2, A.J. GOW1,5, A. PATTIE1,6, J. CORLEY1,6, M.E. BASTIN1,2,
J.M. STARR1, J.M. WARDLAW1,2, I.J. DEARY1,6, E. COMBET7*
1. Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK; 2. Department of Neuroimaging Sciences, Centre for Clinical Brain Sciences,
University of Edinburgh, Edinburgh, UK; 3. Department of Nutrition, University of Aberdeen, Aberdee.
“Cognition is a field of thought processes by which an individual processes information through skills of perception, thinking, memory, learning and attention”
Zinc, the 2nd most abundant trace micronutrient
Almost 40 to 50% vulnerable group are zinc deficient
Zinc deficiency effect cognition development by
Modulating zinc homeostasis
Neurogenesis
Strategies like diet diversification, fortification and supplementation are helpful in alleviating deficiency
Metabolomics: The Next Generation of Biochemistry Metabolon, Inc.
This brief eBook explores the benefits of incorporating the science of metabolomics into contemporary biology research as a stand-alone tool or as a compliment to genomics or other types of molecular biology research.
Biohacker Summit 2022 presentation – 10 Hallmarks of Aging & Reversal Olli Sovijärvi
My comprehensive presentation on the 10 hallmarks of aging and how to reverse aging by targeting these. History of anti-aging research, recent discoveries and lifestyle hacking.
Phenotypic Plasticity, CYP19A1 Pleiotropy, and Maladaptive Selection in Devel...J Patrick Malone
The contribution of evolutionary psychology to the study of development and psychopathology depends on adherence to the principles of evolutionary biology. The human brain evolved because selection favored neither size nor complexity but
instead the phenotypic plasticity supporting cognitive flexibility. Cell proliferation, migration, elongation, synaptogenesis, synaptic pruning, apoptosis, and myelination occur at varying rates during asynchronous phases of development throughout
the brain. Developmentally sensitive periods result from phenotypic plasticity and are vital for adaptation to the environment. The biological systems surrounding the CYP19A1 gene provide mechanisms for neuroprotection and targeted neuronal
debridement in response to environmental stress, uniting selection with developmental biology. Updates to Dunbar’s original hypothesis with current primatological data, inclusion of total brain mass, and the introduction of CYP19A1 orthology from
nine primate species yields a linear regression, R2 = .994, adjusted R2 = .989, F(3, 5) = 143.758, p < .001.
There is Time to Adjust. Aging as a Protective Factor for Autism-Crimson Publ...CrimsonPublishersGGS
There is Time to Adjust. Aging as a Protective Factor for Autism by Diego Iacono in Gerontology & Geriatrics studies
Autism spectrum disorder (ASD) is formally diagnosed before the age of 3 that is, when the central nervous system (CNS) is not yet completely formed, but it is mature enough to generate behavioural abnormalities in some individuals when compared to an age- matched group of typically developed children [1,2]. However, ASD is not a life-threating disease and children diagnosed with ASD age at the same rate as their peers. The possible detrimental or beneficial factors associated with aging in children affected by ASD are not fully known. Surprisingly, the amount of peer-reviewed medical and scientific international literature published on the topic of aging with autism is quite modest and sporadic [3]. The scarcity of aging-ASD investigations derives from the lower level of attention, and related funding opportunities, from the major public and private funding agencies for research across the globe
Presentation slides of a research proposal for using simple eye-tracking system for diagnosis of ADHD.
In collaboration with Hossein Razbarry in the university of Trento. Affective Computing project.
Preliminary ADHD diagnosis using eye-tracking at home
Poster_MKZ
1. • The aging population is rapidly expanding- the number of individuals 65 years and
older will increase from 35 million in 2000 to an estimated 72 million in 2030 [1].
• The brain is particularly vulnerable to the effects of aging, and age-related
deterioration of membrane phospholipids results in cortical thinning [2,3].
• The extent of thinning varies across the cortex, with pronounced structural
degeneration in regions of the prefrontal cortex, which results in selective declines
in cognition [4,5].
• Executive functions (i.e. cognitive flexibility) decline early in normal aging, and
may reflect changes in prefrontal cortex integrity [6, 7].
• Plasma phosphatidylcholine is a marker of age-related membrane degeneration
and is highly predictive of cognitive decline. Thus, phosphatidylcholine shows
promise as a target for nutritional interventions in healthy aging [3,8,9,10,11,12].
1. Decision Neuroscience Laboratory, Beckman Institute for Advanced Science and Technology, University of Illinois Urbana-Champaign, Urbana, IL
2. Abbott Nutrition, Columbus, OH
Hypothesis
Methods
Plasma phosphatidylcholine status will positively associate with cognitive
performance on a measure of executive function (cognitive flexibility), and this
relationship will be mediated by structural integrity of regions within the prefrontal
cortex.
• Subjects: Healthy adults
N = 70, 65-75 years old, average age= 69.05 (SD: 2.84) years
• Biomarker assessment:
Plasma phosphatidylcholine [13]
• Cognitive assessment:
Delis-Kaplin Executive Function System Trail Making Test: Cognitive flexibility [14]
• Structural magnetic resonance imaging
Freesurfer Image Analysis Package: Cortical thickness of prefrontal regions [15]
• Mediation analysis:
1. Multivariate linear regressions
a. Phosphatidylcholine levels à cognitive flexibility
Covariates: age, gender, education, income, BMI, depression
b. Phosphatidylcholine levels à cortical thickness
Covariates: age, gender, education, income, BMI, depression, frontal thickness
2. Sobel z-test [16,17]
Phosphatidylcholine levels + cortical thickness à cognitive flexibility
1. Projections for 2010 through 2050 are from: Table 12. Projections of the Population by Age and Sex for the United States: 2010 to 2050 (NP2008-T12), Population Division, U.S. Census
Bureau; Release Date: August 14, 2008
2. Kosicek, M., and Hecimovic, S. (2013). Phospholipids and Alzheimer’s Disease: Alterations, Mechanisms and Potential Biomarkers. Int. J. Mol. Sci. 14, 1310–1322.
3. Whiley, L., Sen, A., Heaton, J., Proitsi, P., Garcia-Gomez, D., Leung, R., et al. (2014). Evidence of altered phosphatidylcholine metabolism in Alzheimer’s disease. Neurobiol. Aging 35,
271–278.
4. Claassen, D. O., Dobolyi, D. G., Isaacs, D. A., Roman, O. C., Herb, J., Wylie, S. A., et al. (2016). Linear and Curvilinear Trajectories of Cortical Loss with Advancing Age and Disease
Duration in Parkinson’s Disease. Aging Dis. 7, 1–10.
5. Lockhart, S. N., and DeCarli, C. (2014). Structural Imaging Measures of Brain Aging. Neuropsychol. Rev. 24, 271–289.
6. Johnson, J., Lui, L., and Yaffe, K. (2007). Executive function, more than global cognition, predicts functional decline and mortality in elderly women. J. Gerontol. 62, 1134–1141.
7. Yuan, P., and Raz, N. (2014). Neuroscience and Biobehavioral Reviews Prefrontal cortex and executive functions in healthy adults : A meta-analysis of structural neuroimaging studies.
Neurosci. Biobehav. Rev. 42, 180–192.
8. Mapstone, M., Cheema, A. K., Fiandaca, M. S., Zhong, X., Mhyre, T. R., MacArthur, L. H., et al. (2014). Plasma phospholipids identify antecedent memory impairment in older adults.
Nat. Med. 20, 415–8.
9. Norris, S. E., Friedrich, M. G., Mitchell, T. W., Truscott, R. J. W., and Else, P. L. (2015). Human prefrontal cortex phospholipids containing docosahexaenoic acid increase during normal
adult aging, whereas those containing arachidonic acid decrease. Neurobiol. Aging 36, 1659–69.
10. Zeisel, S. H. (2008). Choline: critical role during fetal development and dietary requirements in adults. Annu. Rev. Nutr. 26, 229–250.
11. Frisardi, V., Panza, F., Seripa, D., Farooqui, T., and Farooqui, A. A. (2011). Glycerophospholipids and glycerophospholipid-derived lipid mediators: A complex meshwork in Alzheimer’s
disease pathology. Prog. Lipid Res. 50, 313–330.
12. Wurtman, R. (2015). Biomarkers in the diagnosis and management of Alzheimer’s disease. Metab. Clin. Exp. 4, 547–550.
13. Koc, H., Mar, M. H., Ranasinghe, A., Swenberg, J. A., and Zeisel, S. H. (2002). Quantitation of choline and its metabolites in tissues and foods by liquid chromatography/electrospray
ionization-isotope dilution mass spectrometry. Anal. Chem. 74, 4734–4740.
14. Delis, D. C., Kaplan, E., and Kramer, J. H. (2006). TEST REVIEW: Delis Kaplan Executive Function System (D-KEFS). Appl. Neuropsychol. 13.
15. http://surfer.nmr.mgh.harvard.edu/
16. Baron, R. M., and Kenny, D. A. (1986). The moderator–mediator variable distinction in social psychological research: Conceptual, strategic, and statistical considerations. J. Pers. Soc.
Psychol. 51, 1173–1182.
17. Zhao, X., Lynch Jr., J. G., and Chen, Q. (2010). Reconsidering Baron and Kenny: Myths and Truths about Mediation Analysis. J. Consum. Res. 37, 197–206.
18. Jerneren, F., Elshorbagy, A. K., Oulhaj, A., Smith, S. M., Refsum, H., and Smith, A. D. (2015). Brain atrophy in cognitively impaired elderly : the importance of long-chain w-3 fatty acids
and B vitamin status in a randomized. Am. J. Clin. Nutr., 215–21.
19. Cole, G.M. & Frautschy, S.A. (2010). DHA may prevent age-related dementia. J. Nutr. 140, 869-874.
20. Blusztajn, J. K., Liscovitch, M., and Richardson, U. I. (1987). Synthesis of acetylcholine from choline derived from phosphatidylcholine in a human neuronal cell line. Proc. Natl. Acad.
Sci. U. S. A. 84, 5474–5477.
21. Cohen, B. M., Renshaw, P. F., Stoll, A. L., Wurtman, R. J., Yurgelun-todd, D., and Babb, S. M. (1995). Decreased Brain Choline in Older Adults. Jama 274, 902–907.
FUNDING:
Center for Nutrition, Learning, and Memory
UIUC Neuroscience Program
CONTACT: mzamro2@illinois.edu
Results & Discussion
Objective:
Investigate the neural mechanisms that mediate the relationship
between phosphatidylcholine and cognitive decline in normal aging
Conclusions:
Phosphatidylcholine may slow age-related decline in cognitive
flexibility by preserving structural integrity of inferior prefrontal cortex
Multivariate linear regressions
Future directions
• What mechanisms allow for specific nutrients to target particular brain
regions and therefore selectively influence cognitive decline?
• How can we further characterize such specific and sensitive relationships
between nutrition, cognition, and brain health to inform targeted treatment
of cognitive and neurological impairments of the aging brain?
Results:
Inferior prefrontal cortex thickness mediates the relationship
between phosphatidylcholine levels and cognitive flexibility
References
Phosphatidylcholine Cognitive flexibility
Prefrontal cortex
thickness
2.00!
2.10!
2.20!
2.30!
2.40!
2.50!
2.60!
2.70!
1000! 1500! 2000! 2500! 3000! 3500!
InferiorPrefrontalCortexThickness(mm)!
Phosphatidylcholine (uM)!
0!
2!
4!
6!
8!
10!
12!
14!
1000! 1500! 2000! 2500! 3000! 3500!
CognitiveFlexibilityScore!
Phosphatidylcholine (uM)!
Sobel Z-test
Mediating variable
(Left inferior prefrontal cortex thickness)
Independent variable
(Phosphatidylcholine)
Dependent variable
(Cognitive flexibility)
t = 1.953
p = 0.025
β = 0.672
p = 0.232
β = 7.047
p = 0.003
β = 0.672
p = 0.035
β = 0.043
p = 0.015
Phosphatidylcholine
Cognitive flexibility
Phosphatidylcholine
Inferior prefrontal
cortex thickness
Phosphatidylcholine
Potential mechanisms
2
1
4
3
6
5
2
1
A
B
3
C
Long-chain
polyunsaturated fats
Choline
Membrane integrity
[2]
Anti-inflammatory
effects [19]
Acetylcholine
projections [20,21]