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Effects of Dietary Patterns and Lifestyle on Neurodegenerative Diseases

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

Deadline for manuscript submissions: closed (25 January 2024) | Viewed by 7453

Special Issue Editors


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Guest Editor
1. Department of Exercise and Health Promotion, College of Kinesiology and Health, Chinese Culture University, Taipei 11114, Taiwan
2. Department of Neurology, Chang Bing Show Chwan Memorial Hospital, Changhua County 50544, Taiwan
Interests: neurodegenerative diseases; stroke, autonomic nervous system disorders; neuroimage

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Guest Editor
Institute of Biomedical Engineering, School of Life Science, Shanghai University, Shanghai 200444, China
Interests: Alzheimer's disease; Parkinson's diseas; dementia; neurodegenerative disorders; medical imaging processing; biomedical engineering
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases include Alzheimer’s disease (AD), Parkinson’s disease (PD), parkinsonian syndromes, and amyotrophic lateral sclerosis (ALS), etc. The established risk factors of neurodegenerative diseases include certain genetic polymorphisms and aging. Other possible causes may include gender, poor education, endocrine conditions, oxidative stress, inflammation, stroke, hypertension, diabetes, smoking, traumatic brain injury (TBI), depression, infection, tumors, immune and metabolic conditions, and environmental pollution. Moreover, various lifestyle risk factors, including sleep, physical activity and an individual’s dietary pattern, are garnering greater attention.

The aim of this Special Issue is to assemble the latest research on these topics. Therefore, original studies, narrative and systematic reviews, and meta-analyses that attend to the effects of sleep duration, physical activity, and dietary patterns on neurodegenerative diseases are most welcome.

Dr. Cheng-Yu Wei
Dr. Jiehui Jiang
Guest Editors

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Keywords

  • Alzheimer’s disease
  • Parkinson’s disease
  • Parkinsonian syndromes
  • neurodegenerative diseases
  • amyotrophic lateral sclerosis
  • dietary pattern
  • sleep
  • physical activity

Published Papers (3 papers)

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Research

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16 pages, 2398 KiB  
Article
Efficacy of Probiotic Supplements on Brain-Derived Neurotrophic Factor, Inflammatory Biomarkers, Oxidative Stress and Cognitive Function in Patients with Alzheimer’s Dementia: A 12-Week Randomized, Double-Blind Active-Controlled Study
by Yu-Chieh Hsu, Yen-Yu Huang, Shin-Yu Tsai, Yi-Wei Kuo, Jia-Hung Lin, Hsieh-Hsun Ho, Jui-Fen Chen, Ko-Chiang Hsia and Yu Sun
Nutrients 2024, 16(1), 16; https://0-doi-org.brum.beds.ac.uk/10.3390/nu16010016 - 20 Dec 2023
Cited by 3 | Viewed by 2555
Abstract
The role of neurotrophic factors, oxidative stress, and inflammation in the pathogenesis of Alzheimer’s disease (AD) has been explored. Animal studies have reported the positive effects of probiotics on these factors. Some clinical studies also support the potential role of probiotics in improving [...] Read more.
The role of neurotrophic factors, oxidative stress, and inflammation in the pathogenesis of Alzheimer’s disease (AD) has been explored. Animal studies have reported the positive effects of probiotics on these factors. Some clinical studies also support the potential role of probiotics in improving cognitive function via the gut–brain axis in older adults. However, clinical experimental studies evaluating the efficacy of probiotics targeting the neurotrophic factors and inflammatory biomarkers, particularly among AD patients, remain very limited. In this randomized, double-blinded, active-controlled trial, we used multi-strain probiotic supplements, including Bifidobacterium longum subsp. infantis BLI-02, B. breve Bv-889, B. animalis subsp. lactis CP-9, B. bifidum VDD088, and Lactobacillus plantarum PL-02 as the intervention. Participants were divided into an active control group (received probiotic supplements containing 5 × 107 colony-forming units per day, CFU/day) and a treatment group (1 × 1010 CFU/day). Student’s t test was applied as the main method of statistical analysis. After 12 weeks of intervention, the treatment group demonstrated a 36% increase in serum brain-derived neurotrophic factor (BDNF) (* p = 0.005), a reduction in IL-1β (* p = 0.041), and an increase in antioxidant superoxide dismutase (SOD) (* p = 0.012). No significant change was found in the active control group. A trend toward less cognitive deterioration was observed, but not statistically significant. In conclusion, this study presents evidence supporting the benefits of multi-strain probiotics in enhancing BDNF, ameliorating inflammation and oxidative stress in AD patients. Full article
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12 pages, 949 KiB  
Article
Cholesterol Levels, Hormone Replacement Therapy, and Incident Dementia among Older Adult Women
by Huei-Ying Chiu, Hsin-Te Chang, Po-Chi Chan and Pai-Yi Chiu
Nutrients 2023, 15(20), 4481; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15204481 - 23 Oct 2023
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Abstract
Previous studies revealed that hormone replacement therapy (HRT) probably has a protective effect for preventing dementia in post-menopausal women. However, the results were still controversial. The association between cholesterol levels and incident dementia in older women is not fully understood either. We conducted [...] Read more.
Previous studies revealed that hormone replacement therapy (HRT) probably has a protective effect for preventing dementia in post-menopausal women. However, the results were still controversial. The association between cholesterol levels and incident dementia in older women is not fully understood either. We conducted a retrospective analysis on a cohort of non-demented women aged older than 50 years, which was registered in the History-based Artificial Intelligence Clinical Dementia Diagnostic System database from September 2015 to August 2021. We followed this cohort longitudinally to examine the rates of conversion to dementia. Using a Cox regression model, we investigated the impact of the quartile of total cholesterol (TC) levels on incident dementia, adjusting for age, sex, education, neuropsychiatric symptoms, neuropsychological assessments, HRT, as well as various vascular risk factors and medications. We examined a cohort of 787 participants, comprising 539 (68.5%) individuals who did not develop dementia (non-converters). Among these non-converters, 68 individuals (12.6%) were treated with HRT. By contrast, there were 248 (31.5%) who did develop dementia (converters). Among the converters, 28 individuals (11.3%) were treated with HRT. The average follow-up durations were 2.9 ± 1.5 and 3.3 ± 1.6 years for non-converters and converters, respectively. Compared to the lowest quartile of TC levels (<153), the hazard ratios (HR) for converting to dementia were 0.61, 0.58, and 0.58 for the second (153–176), third (177–201), and highest (>201) quartiles, respectively (all p < 0.05). However, the low-density lipoprotein cholesterol (LDL-C) level and HRT did not alter the rate of conversion to dementia. In conclusion, the lowest quartile of TC increased incident dementia in post-menopausal women without dementia; however, HRT did not contribute to conversion to dementia. Some studies suggest that post-menopausal women who have reduced estrogen levels might have an increased risk of Alzheimer’s disease if they also have high cholesterol. Nonetheless, the evidence is inconclusive, as not all studies support this finding. The “Lower LDL-C is better” strategy for preventing cardiac vascular disease should be re-examined for the possible serial adverse effects of new onset dementia due to very low cholesterol levels. Full article
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Review

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17 pages, 366 KiB  
Review
Neuroimmunological Effect of Vitamin D on Neuropsychiatric Long COVID Syndrome: A Review
by Ting-Bin Chen, Ching-Mao Chang, Cheng-Chia Yang, I-Ju Tsai, Cheng-Yu Wei, Hao-Wen Yang and Chun-Pai Yang
Nutrients 2023, 15(17), 3802; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15173802 - 30 Aug 2023
Cited by 3 | Viewed by 2576
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the coronavirus disease 2019 (COVID-19). COVID-19 is now recognized as a multiorgan disease with a broad spectrum of manifestations. A substantial proportion of individuals who have recovered from COVID-19 are experiencing [...] Read more.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the coronavirus disease 2019 (COVID-19). COVID-19 is now recognized as a multiorgan disease with a broad spectrum of manifestations. A substantial proportion of individuals who have recovered from COVID-19 are experiencing persistent, prolonged, and often incapacitating sequelae, collectively referred to as long COVID. To date, definitive diagnostic criteria for long COVID diagnosis remain elusive. An emerging public health threat is neuropsychiatric long COVID, encompassing a broad range of manifestations, such as sleep disturbance, anxiety, depression, brain fog, and fatigue. Although the precise mechanisms underlying the neuropsychiatric complications of long COVID are presently not fully elucidated, neural cytolytic effects, neuroinflammation, cerebral microvascular compromise, breakdown of the blood–brain barrier (BBB), thrombosis, hypoxia, neurotransmitter dysregulation, and provoked neurodegeneration are pathophysiologically linked to long-term neuropsychiatric consequences, in addition to systemic hyperinflammation and maladaptation of the renin–angiotensin–aldosterone system. Vitamin D, a fat-soluble secosteroid, is a potent immunomodulatory hormone with potential beneficial effects on anti-inflammatory responses, neuroprotection, monoamine neurotransmission, BBB integrity, vasculometabolic functions, gut microbiota, and telomere stability in different phases of SARS-CoV-2 infection, acting through both genomic and nongenomic pathways. Here, we provide an up-to-date review of the potential mechanisms and pathophysiology of neuropsychiatric long COVID syndrome and the plausible neurological contributions of vitamin D in mitigating the effects of long COVID. Full article
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