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Nutrition and Brain Health

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Public Health".

Deadline for manuscript submissions: closed (20 October 2023) | Viewed by 18760

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Guest Editor
Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, 680 N Lake Shore Drive, Suite 1400, Chicago, IL 60611, USA
Interests: caffeine; coffee; taste; diet behaviours; precison nutrition; genetics; omics; cardiometabolic traits; dementia; aging
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Special Issue Information

Dear Colleagues,

Epidemiological and experimental studies provide evidence regarding the key role of nutrition in brain health, but the specific mechanisms behind its effects are unclear. Recent advancements in omic technology along with the creation of a scientific environment that supports the collection and sharing of data and biospecimens from large cohorts and clinical trials has accelerated the pace of scientific discoveries in this field. For this Special Issue, we invite researchers to showcase the application of omics and existing resources to the study of nutrition and the brain—specifically, neurodegenerative diseases and related traits. Hypothesis-generating studies of nutrients and non-nutrients involving humans or animals are welcome. The submission of hypothesis-testing studies of established omic markers of nutrient response and neurodegeneration is also encouraged.

Dr. Marilyn Cornelis
Guest Editor

Manuscript Submission Information

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Keywords

  • precision nutrition
  • neurodegeneration
  • cognition
  • metabolomics
  • proteomics
  • nutrigenomics
  • biomarkers

Published Papers (7 papers)

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Research

14 pages, 2146 KiB  
Article
Calcium Homeostasis and Psychiatric Disorders: A Mendelian Randomization Study
by Miaomiao Jiang, Weiheng Yan, Xianjing Li, Liyang Zhao, Tianlan Lu, Dai Zhang, Jun Li and Lifang Wang
Nutrients 2023, 15(18), 4051; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15184051 - 19 Sep 2023
Viewed by 1852
Abstract
Observational studies have investigated the impact of calcium homeostasis on psychiatric disorders; however, the causality of associations is yet to be established. Bidirectional Mendelian randomization (MR) analysis of calcium homeostasis hormones was conducted on nine psychiatric disorders. Calcium, serum 25-hydroxyvitamin D levels (25OHD), [...] Read more.
Observational studies have investigated the impact of calcium homeostasis on psychiatric disorders; however, the causality of associations is yet to be established. Bidirectional Mendelian randomization (MR) analysis of calcium homeostasis hormones was conducted on nine psychiatric disorders. Calcium, serum 25-hydroxyvitamin D levels (25OHD), parathyroid hormone, and fibroblast growth factor 23 are the major calcium homeostasis hormones. The causality was evaluated by the inverse variance weighted method (IVW) and the MR Steiger test, while Cochran’s Q test, the MR-Egger intercept test, funnel plot, and the leave-one-out method were used for sensitivity analyses. Bonferroni correction was used to determine the causative association features (p < 6.94 × 10−4). Schizophrenia (SCZ) was significantly associated with decreased 25OHD concentrations with an estimated effect of −0.0164 (Prandom-effect IVW = 2.39 × 10−7). In the Multivariable MR (MVMR) analysis adjusting for potentially confounding traits including body mass index, obesity, mineral supplements (calcium, fish oil, and vitamin D) and outdoor time (winter and summer), the relationship between SCZ and 25OHD remained. The genetically predicted autism spectrum disorder and bipolar disorder were also nominally associated with decreased 25OHD. This study provided evidence for a causal effect of psychiatric disorders on calcium homeostasis. The clinical monitoring of 25OHD levels in patients with psychiatric disorders is beneficial. Full article
(This article belongs to the Special Issue Nutrition and Brain Health)
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14 pages, 2399 KiB  
Article
Oral Treatment with the Extract of Euterpe oleracea Mart. Improves Motor Dysfunction and Reduces Brain Injury in Rats Subjected to Ischemic Stroke
by Leonan Lima Teixeira, Helma Maria Negrão da Silva Alencar, Luan Oliveira Ferreira, João Cleiton Martins Rodrigues, Rafael Dias de Souza, Laine Celestino Pinto, Nilton Akio Muto, Hervé Rogez, Arnaldo Jorge Martins-Filho, Vanessa Joia de Mello, Moises Hamoy, Edmar Tavares da Costa and Dielly Catrina Favacho Lopes
Nutrients 2023, 15(5), 1207; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15051207 - 28 Feb 2023
Cited by 2 | Viewed by 1395
Abstract
Ischemic stroke is one of the principal causes of morbidity and mortality around the world. The pathophysiological mechanisms that lead to the formation of the stroke lesions range from the bioenergetic failure of the cells and the intense production of reactive oxygen species [...] Read more.
Ischemic stroke is one of the principal causes of morbidity and mortality around the world. The pathophysiological mechanisms that lead to the formation of the stroke lesions range from the bioenergetic failure of the cells and the intense production of reactive oxygen species to neuroinflammation. The fruit of the açaí palm, Euterpe oleracea Mart. (EO), is consumed by traditional populations in the Brazilian Amazon region, and it is known to have antioxidant and anti-inflammatory properties. We evaluated whether the clarified extract of EO was capable of reducing the area of lesion and promoting neuronal survival following ischemic stroke in rats. Animals submitted to ischemic stroke and treated with EO extract presented a significant improvement in their neurological deficit from the ninth day onward. We also observed a reduction in the extent of the cerebral injury and the preservation of the neurons of the cortical layers. Taken together, our findings indicate that treatment with EO extract in the acute phase following a stroke can trigger signaling pathways that culminate in neuronal survival and promote the partial recovery of neurological scores. However, further detailed studies of the intracellular signaling pathways are needed to better understand the mechanisms involved. Full article
(This article belongs to the Special Issue Nutrition and Brain Health)
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17 pages, 339 KiB  
Article
MIND Dietary Pattern and Its Association with Cognition and Incident Dementia in the UK Biobank
by Marilyn C. Cornelis, Puja Agarwal, Thomas M. Holland and Rob M. van Dam
Nutrients 2023, 15(1), 32; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15010032 - 21 Dec 2022
Cited by 7 | Viewed by 3894
Abstract
A high adherence to the Mediterranean-Dietary Approaches to Stop Hypertension Diet Intervention for Neurodegenerative Delay (MIND) has been associated with better cognition and a lower risk of dementia in some but not all studies. We measured adherence to MIND and its association with [...] Read more.
A high adherence to the Mediterranean-Dietary Approaches to Stop Hypertension Diet Intervention for Neurodegenerative Delay (MIND) has been associated with better cognition and a lower risk of dementia in some but not all studies. We measured adherence to MIND and its association with cognitive health in the UK Biobank (UKB). A MIND score was derived from 24 h diet recall questionnaires for 120,661 participants who completed at least one of seven self-administered cognitive function tests. In a subset of 78,663 participants aged 55+, diagnosis of dementia was determined by linked hospital and death records. Multivariable regression and Cox proportional hazard ratio (HR) models were used to examine associations of MIND with cognitive ability and incident dementia. Higher adherence to MIND was associated with a small but significant worsening in performance on five of seven cognitive tests (p < 0.002). Associations were strongest among highly educated participants (p < 0.002 for MIND × education interaction). After a mean follow-up time of 10.5 years, 842 participants developed dementia. Overall, MIND adherence was not associated with incident dementia. An inverse association was observed among females (HR = 0.87 per score standard deviation (SD), p = 0.008) but not males (HR = 1.09, p = 0.11) (p = 0.008 for MIND × sex interaction). Similar associations with cognitive ability and dementia were observed for the Alternative Healthy Eating Index-2010 (AHEI-2010) dietary pattern. Associations were not modified by genetic susceptibility. In UKB, the MIND diet was not associated with better cognitive test scores and only with lower dementia risk in women. Full article
(This article belongs to the Special Issue Nutrition and Brain Health)
18 pages, 1309 KiB  
Article
Cognitive Decline Related to Diet Pattern and Nutritional Adequacy in Alzheimer’s Disease Using Surface-Based Morphometry
by Hua-Tsen Hsiao, Mi-Chia Ma, Hsin-I Chang, Ching-Heng Lin, Shih-Wei Hsu, Shu-Hua Huang, Chen-Chang Lee, Chi-Wei Huang and Chiung-Chih Chang
Nutrients 2022, 14(24), 5300; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14245300 - 13 Dec 2022
Cited by 2 | Viewed by 2101
Abstract
Dietary pattern (DP) results in nutrition adequacy and may influence cognitive decline and cortical atrophy in Alzheimer’s disease (AD). The study explored DP in 248 patients with AD. Two neurobehavioral assessments (intervals 13.4 months) and two cortical thickness measurements derived from magnetic resonance [...] Read more.
Dietary pattern (DP) results in nutrition adequacy and may influence cognitive decline and cortical atrophy in Alzheimer’s disease (AD). The study explored DP in 248 patients with AD. Two neurobehavioral assessments (intervals 13.4 months) and two cortical thickness measurements derived from magnetic resonance images (intervals 26.5 months) were collected as outcome measures. Reduced rank regression was used to assess the groups of DPs and a linear mixed-effect model to explore the cortical neurodegenerative patterns. At screening, underweight body mass index (BMI) was related to significant higher lipid profile, impaired cognitive function, smaller cortical thickness, lower protein DP factor loading scores and the non-spouse caregiver status. Higher mini-mental state examination (MMSE) scores were related to the DP of coffee/tea, compared to the lipid/sugar or protein DP group. The underweighted-BMI group had faster cortical thickness atrophy in the pregenual and lateral temporal cortex, while the correlations between cortical thickness degeneration and high HbA1C or low B12 and folate levels were localized in the medial and lateral prefrontal cortex. The predictive model suggested that factors related to MMSE score were related to the caregiver status. In conclusion, normal or overweight BMI, coffee/tea DP group and living with a spouse were considered as protective factors for better cognitive outcomes in patients with AD. The influence of glucose, B12 and folate on the cortical degeneration was spatially distinct from the pattern of AD degeneration. Full article
(This article belongs to the Special Issue Nutrition and Brain Health)
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20 pages, 4842 KiB  
Article
Gut Microbiota Dysbiosis after Traumatic Brain Injury Contributes to Persistent Microglial Activation Associated with Upregulated Lyz2 and Shifted Tryptophan Metabolic Phenotype
by Zhipeng Zheng, Shuai Wang, Chenghao Wu, Yang Cao, Qiao Gu, Ying Zhu, Wei Zhang and Wei Hu
Nutrients 2022, 14(17), 3467; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14173467 - 24 Aug 2022
Cited by 11 | Viewed by 2344
Abstract
Traumatic brain injury (TBI) is a common cause of disability and mortality, affecting millions of people every year. The neuroinflammation and immune response post-TBI initially have neuroprotective and reparative effects, but prolonged neuroinflammation leads to secondary injury and increases the risk of chronic [...] Read more.
Traumatic brain injury (TBI) is a common cause of disability and mortality, affecting millions of people every year. The neuroinflammation and immune response post-TBI initially have neuroprotective and reparative effects, but prolonged neuroinflammation leads to secondary injury and increases the risk of chronic neurodegenerative diseases. Persistent microglial activation plays a critical role in chronic neuroinflammation post-TBI. Given the bidirectional communication along the brain–gut axis, it is plausible to suppose that gut microbiota dysbiosis post-TBI influences microglial activation. In the present study, hippocampal microglial activation was observed at 7 days and 28 days post-TBI. However, in TBI mice with a depletion of gut microbiota, microglia were activated at 7 days post-TBI, but not at 28 days post-TBI, indicating that gut microbiota contributes to the long-term activation of microglia post-TBI. In addition, in conventional mice colonized by the gut microbiota of TBI mice using fecal microbiota transplant (FMT), microglial activation was observed at 28 days post-TBI, but not at 7 days post-TBI, supporting the role of gut microbiota dysbiosis in persistent microglial activation post-TBI. The RNA sequencing of the hippocampus identified a microglial activation gene, Lyz2, which kept upregulation post-TBI. This persistent upregulation was inhibited by oral antibiotics and partly induced by FMT. 16s rRNA gene sequencing showed that the composition and function of gut microbiota shifted over time post-TBI with progressive dysbiosis, and untargeted metabolomics profiling revealed that the tryptophan metabolic phenotype was differently reshaped at 7 days and 28 days post-TBI, which may play a role in the persistent upregulation of Lyz2 and the activation of microglia. This study implicates that gut microbiota and Lyz2 are potential targets for the development of novel strategies to address persistent microglial activation and chronic neuroinflammation post-TBI, and further investigations are warranted to elucidate the specific mechanism. Full article
(This article belongs to the Special Issue Nutrition and Brain Health)
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15 pages, 1084 KiB  
Article
Adherence to MIND Diet, Genetic Susceptibility, and Incident Dementia in Three US Cohorts
by Thanh Huyen T. Vu, Todd Beck, David A. Bennett, Julie A. Schneider, Kathleen M. Hayden, Aladdin H. Shadyab, Kumar B. Rajan, Martha Clare Morris and Marilyn C. Cornelis
Nutrients 2022, 14(13), 2759; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14132759 - 03 Jul 2022
Cited by 11 | Viewed by 4062
Abstract
Adherence to Mediterranean-DASH Diet Intervention for Neurodegenerative Delay (MIND) may lower the risk of dementia by impacting immunity and cholesterol, which are pathways also implicated by genome-wide association studies of Alzheimer’s Dementia (AD). We examined whether adherence to the MIND diet could modify [...] Read more.
Adherence to Mediterranean-DASH Diet Intervention for Neurodegenerative Delay (MIND) may lower the risk of dementia by impacting immunity and cholesterol, which are pathways also implicated by genome-wide association studies of Alzheimer’s Dementia (AD). We examined whether adherence to the MIND diet could modify the association of genetic risk for AD with incident dementia. We used three ongoing US cohorts: Chicago Health and Aging Project (CHAP, n = 2449), Rush Memory and Aging Project (MAP, n = 725), and Women’s Health Initiative Memory Study (WHIMS, n = 5308). Diagnosis of dementia was based on clinical neurological examination and standardized criteria. Repeated measures of global cognitive function were available in MAP and CHAP. Self-reported adherence to MIND was estimated using food-frequency questionnaires. Global and pathway-specific genetic scores (GS) for AD were derived. Cox proportional hazard, logistic regression, and mixed models were used to examine associations of MIND, GS, and GS-MIND interactions with incident dementia and cognitive decline. Higher adherence to MIND and lower GS were associated with a lower risk of dementia in MAP and WHIMS and a slower rate of cognitive decline in MAP (p < 0.05). MIND or GS were not associated with incident dementia or cognitive decline in CHAP. No gene–diet interaction was replicated across cohorts. Genetic risk and MIND adherence are independently associated with dementia among older US men and women. Full article
(This article belongs to the Special Issue Nutrition and Brain Health)
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10 pages, 615 KiB  
Article
Association between Geriatric Nutritional Risk Index and Depression after Ischemic Stroke
by Jianian Hua, Jieyi Lu, Xiang Tang and Qi Fang
Nutrients 2022, 14(13), 2698; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14132698 - 29 Jun 2022
Cited by 7 | Viewed by 2205
Abstract
Background: Malnutrition is associated with poor outcomes after stroke. However, the association between malnutrition and post-stroke depression (PSD) remains unelucidated. We aimed to explore the association between geriatric nutritional risk index (GNRI) and depression after ischemic stroke. Methods: In total, 344 patients with [...] Read more.
Background: Malnutrition is associated with poor outcomes after stroke. However, the association between malnutrition and post-stroke depression (PSD) remains unelucidated. We aimed to explore the association between geriatric nutritional risk index (GNRI) and depression after ischemic stroke. Methods: In total, 344 patients with ischemic stroke were included in this analysis. The GNRI was calculated from serum albumin level, weight, and height at admission. Malnutrition was defined using the GNRI cutoff points. A lower GNRI score indicates an elevated nutritional risk. The outcome was depression, measured 14 days after ischemic stroke. Logistic regression models were used to estimate the association between the GNRI and risk of PSD. Results: A total of 22.9% developed PSD 14 days after stroke. The mean GNRI was 99.3 ± 6.0, and 53.8% of the patients had malnutrition. After adjusting for covariates, baseline malnutrition was not associated with risk of PSD (OR, 0.670; 95%CI, 0.370–1.213; p = 0.186). The restricted cubic splines revealed a U-shaped association between the GNRI and PSD. Compared to moderate GNRI, higher GNRI (OR, 2.368; 95%CI, 0.983–5.701; p = 0.085) or lower GNRI (OR, 2.226; 95%CI, 0.890–5.563; p = 0.087) did not significantly increase the risk of PSD. Conclusion: A low GNRI was not associated with an increased risk of depression after ischemic stroke. Full article
(This article belongs to the Special Issue Nutrition and Brain Health)
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