Nutritional Neuroscience最新文献

Objectives: The gut microbiota refers to a complex and essential ecosystem comprised of over 100 trillion microbial cells. The microbiota, the gut, and the brain together create an association which is vital to host health, 'the microbiota-gut-brain axis,' and coordinate the gut with the central nervous system to modify cognitive function and brain immune homeostasis. This bidirectional talk between the gut and brain operates via the immune system, the enteric nervous system, as well as various microbial metabolites, including short-chain fatty acids (SCFAs), and proteins. Recent studies have suggested an important role for the gut microbiota in many neurodegenerative diseases, including Alzheimer's disease (AD). The neuropathological hallmarks of Alzheimer's disease consist of beta-amyloid plaques, tau hyperphosphorylation, neurofibrillary tangles, glial activation, and neuronal and synaptic loss.

Methods: In this narrative review, we summarize the major outcomes of recent studies investigating the impacts of nutrition interventions, exercise interventions, and combined lifestyle (exercise + nutrition) interventions on Alzheimer's pathophysiology in animal models.

Results: Collectively, the interventions reviewed here all achieved significantly improved measures of cognitive function, beta-amyloid plaque aggregation and glial responses in the rodents, and led to the alterations in gut microbial composition, changes in bacterial metabolites, neuroinflammation, synaptic plasticity, and blood-brain barrier integrity.

Discussion: Understanding the role of the microbiota-gut-brain axis pathways during lifestyle interventions discussed in this study may assist in providing novel targets to delay the onset and progression of AD or alleviate extant AD pathophysiology, and may promote a reduction in the prevalence of AD.

Objectives: There is a serious conflict in the literature regarding the relationship between Omega-3 fatty acids and the risk of Alzheimer's disease. Additionally, the relationship between Alzheimer's and dietary omega-3 fatty acids has not been explored in the Middle East region.

Methods: This study aimed to evaluate the association between dietary omega-3 fatty acids and the risk of Alzheimer's disease. The study included 301 participants (150 cases and 151 controls). Cases were recruited among people in the early stages of the disease who had been diagnosed with Alzheimer's disease within the past six months. Controls were selected from health centres across Tehran. Dietary intake was assessed using the validated 168-item food frequency questionnaire.

Results: After adjusting for potential cofounders, individuals in the third tertile of total dietary omega-3 fatty acids had 64 percent lower chance of Alzheimer's disease (OR: 0.36, 95% CI: 0.18-0.74). Among women, compared to the lowest tertile, female subjects in the third tertile of total omega-3 fatty acids intake had an odds ratio of 0.22 for Alzheimer's disease (OR: 0.22, 95% CI: 0.08-0.63). Yet, within the group of participants experiencing overweight or obesity, the adjusted models show no significant association between omega-3 fatty acid intake and risk of Alzheimer's disease.

Discussion: In summary, our findings indicated that higher dietary omega-3 fatty acids might be associated with a decreased risk of Alzheimer's disease. However, further research is required to explore the relationship between dietary omega-3 fatty acids and Alzheimer's disease.

Objectives: Neuroinflammation contributes to the pathogenesis of multiple neurological and neurodegenerative diseases but is also involved in non-degenerative conditions such as aging, sleep disorders, depression, and metabolic dysfunctions. Among dietary factors with potential neuroprotective activity, olive oil and its phenolic compounds have attracted interest for their anti-inflammatory properties. This systematic review aimed to assess the effects of olive oil and its main phenolic compounds on neuroinflammation in preclinical in vivo studies.

Methods: A systematic search was conducted using PubMed, Scopus, and Web of Science to identify controlled in vivo studies evaluating the impact of olive oil or its phenolic compounds on neuroinflammatory markers. Thirty-two studies met the inclusion criteria and were critically analyzed for experimental model, type of intervention, and neuroinflammation-related outcomes.

Results: Olive oil, particularly extra-virgin olive oil (EVOO) rich in phenolic compounds, showed anti-inflammatory effects in several models, although results were inconsistent. In contrast, phenolic compounds such as hydroxytyrosol, oleuropein, oleacein, and oleocanthal more consistently reduced glial activation and pro-inflammatory cytokines across diverse experimental paradigms. Hydroxytyrosol emerged as the most frequently studied and effective compound.

Discussion: The preclinical evidence supports the anti-neuroinflammatory potential of olive oil and its phenolic compounds, though the variability in experimental design, compound characterization, and outcome measures limits translational interpretation. While isolated compounds demonstrated more robust effects than whole oil, high doses and lack of pharmacokinetic data raise questions about clinical relevance. Future research should address these limitations and evaluate the neuroimmune effects of olive oil-derived compounds in human studies.

Tolerogenic probiotics, including Lactobacillus and Bifidobacterium species, offer significant therapeutic potential for neuroimmune disorders by modulating the gut-brain axis to promote immune tolerance and reduce inflammation. These probiotics influence key cell types, such as enteroendocrine cells (EECs), intestinal epithelial cells (IECs), and enteric glial cells (EGCs), enhancing gut barrier integrity and regulating hormone secretion (e.g. GLP-1, serotonin). They also modulate pain receptors, including transient receptor potential vanilloid 1 (TRPV1), cannabinoid (CB1, CB2), opioid (mu, kappa), and serotonin (5-HT) receptors, to alleviate visceral and neuropathic pain hypersensitivity. Despite promising preclinical evidence, challenges such as inconsistent dosing protocols, strain-specific efficacy, and limited large-scale clinical trials hinder clinical translation. This review synthesizes the mechanisms by which tolerogenic probiotics target the gut-brain axis and pain receptors, highlighting research gaps and proposing directions for personalized therapies and standardized clinical approaches.

The gut-brain axis explains that changes in the intestinal microbiota influence Alzheimer's disease (AD). Short-chain fatty acids produced by the gut microbiome regulate the permeability of the gut and blood-brain barrier. Furthermore, they upregulate brain-derived neurotrophic factor, promote angiogenesis and neurogenesis, and control tau and Aβ proteins, microglial activity, apoptosis, oxidative damage, M1/M2 polarization of microglia, and neuroinflammation, which eventually improves cognitive impairment. This effect is mediated by modification of serotonin, dopamine, and γ-aminobutyric acid levels. Compared to healthy controls, mild cognitive impairment and AD were associated with low levels of Firmicutes and Bifidobacterium and high levels of Proteobacteria and Bacteroidetes. Lactobacillus and Bifidobacterium species were effective in improving cognitive function. More longitudinal research is needed to investigate precision medicine in patients with dysbiosis in the preclinical stages of the disease. This review describes the role of the gut microbiome and probiotics in AD.

Objectives: There is a significant need to reduce sugar in food. We can replace sugar with non-nutrient sweeteners; however, they need to be desirable. Previously, we found adding a flavour modifier to a taste can result in neural super-additivity that could drive enhanced pleasure. It is not known if adding a flavour modifier to a non-nutrient sweetener could affect brain activity in the same way.

Methods: Healthy adults (N = 48, Mean age 26 yrs.) participated. We examined the neural effects of adding a flavour modifier to the non-nutrient sweetener sucralose (SLM) and the neural effects of sucrose vs sucralose. We examined whole brain data and the ROIs insula, pre- and postcentral gyrus, identified from a meta-analysis on brain responses to sweet tastes.

Results: Super-additive neural effects to SLM were in the mid/inferior temporal gyri, pre- and post-central gyri and parietal areas at the whole-brain level, p < 0.05 Family Wise Error corrected threshold. Superior frontal gyrus activity correlated with SLM pleasantness. There were no whole brain differences including reward-related differences between sucrose and sucralose. We did find greater ROI somatosensory activity (p = 0.01) for sucrose vs sucralose.

Discussion: We provide the first evidence that adding a flavour modifier to a non-nutrient sweetener reveals synergistic neural activity in brain areas associated with taste sensation, intensity, attention, perception and multisensory integration. Modifiers added to sweeteners could help consumers switch to healthier options and producers reduce the amount of sugar in foods. Future studies should examine if neural super-additivity effects can be used to predict subsequent consummatory behaviour.

Objectives: This study aimed to investigate the impact of supplementing the maternal cafeteria diet with omega-3 fatty acids (ω3) on serum glucose, insulin, and leptin levels, as well as hypothalamic mRNA expression levels of pro-opiomelanocortin (Pomc), neuropeptide-Y (Npy), agouti-related protein (Agrp), and brain-derived neurotrophic factor (Bdnf) genes in the offspring.

Methods: Pregnant C57BL/6J mice were divided into four groups (n = 8 each): cafeteria diet, cafeteria diet plus ω3 supplementation (300 mg/kg/day), chow diet, and chow diet plus ω3 supplementation. Gestation and lactation were monitored, and blood and tissue samples were collected from 62 offspring.

Results: No significant differences were observed in maternal body weight at pregnancy onset. However, dietary intervention influenced weight gain and intake during gestation and lactation. The cafeteria diet group consumed more energy, fat, saturated fat, and less protein and fiber, with similar carbohydrate intake. This group showed higher serum glucose levels in offspring than the control group, while insulin and leptin levels remained unaffected. Supplementing the maternal cafeteria diet with ω3 had no beneficial effect on serum glucose, insulin, or leptin. Neither the cafeteria diet nor ω3 supplementation altered hypothalamic Pomc, Npy, Agrp, or Bdnf mRNA expression.

Discussion: These findings suggest that the maternal cafeteria diet may adversely affect some biochemical parameters in offspring without inducing short-term changes in nutrition-related gene expression. Ω3 supplementation conferred no apparent therapeutic benefit. Limitations include the absence of adiposity measurements and long-term follow-up, which may have influenced outcomes. Further research is needed to explore long-term metabolic consequences and underlying epigenetic mechanisms.

Objectives: Patients with severe mental illnesses (SMI), such as schizophrenia and depression, face significant challenges in maintaining healthy dietary habits. However, in practice, easily accessible and available options for nutritional support in psychiatric settings remain lacking. This study aimed to identify the specific difficulties faced by these patients and explore the types of support they find most beneficial.

Methods: Using a qualitative, participatory approach we conducted six focus groups with 4-9 patients from the Psychiatric University Hospital Zurich between September and December 2023. The interviews were guided by a pre-developed discussion guideline and analyzed using MAXQDA with qualitative content analysis based on Graneheim and Lundman's approach. A deductive-inductive method was chosen for coding the transcripts.

Results: A total of 38 patients (50% female, 23-61 years, 92% with depression, 5% with schizophrenia, 3% did not state the diagnosis) described a range of difficulties related to meal preparation and cooking, emotional eating, and medical factors, all compounded by overarching problems regarding daily structure and feelings of resignation. Participants were open to a variety of support options, with preference for practical hands-on support from mental health professionals to help translate their knowledge into action (e.g. support with shopping or meal planning). Participants wanted to be actively asked about nutrition problems.

Discussion: The findings highlight the complex interplay of cognitive, emotional, and practical barriers to healthy eating in patients with SMI. There is a need for integrated nutritional support within psychiatric care, emphasizing the importance of practical, personalized, and proactive interventions.

Background: Carotenoids are naturally occurring bio-pigments found in microalgae, plants, fungi, bacteria, and various aquatic animals. They are generally classified into carotenes and xanthophylls based on their structural features. Among them, astaxanthin-a xanthophyll carotenoid-has attracted increasing attention due to its potent antioxidant, anti-inflammatory, and anti-apoptotic properties, which contribute to a range of health benefits.

Method: This review highlights the structural features, physicochemical properties, pharmacokinetics, and therapeutic potential of astaxanthin, particularly focusing on its neuroprotective effects in neurological disorders. To provide a comprehensive overview, we systematically searched published articles across Scopus, Google Scholar, PubMed, and Medline databases from inception to January 1, 2025.

Results: Recent advancements in drug formulation and delivery technologies have enhanced astaxanthin's ability to cross the blood-brain barrier (BBB), significantly increasing its potential as a therapeutic agent for neurological diseases.

Conclusion: With its multifaceted biological effects and growing evidence of neuroprotection, astaxanthin shows great promise in the treatment of neurological disorders, particularly stroke. These findings support its future development and application in pharmaceutical strategies aimed at brain health.

Background: Alzheimer's disease (AD) is a multi-factorial type of dementia that poses a social and medical burden in that no effective treatment has been achieved yet. Impaired brain glucose metabolism is one of the major pathophysiological factors linked to its onset and progression. Lauric acid (LA) is a triglyceride with medium chain that can produce ketone body utilize by the brain as an alternative energy source.Objective: Therefore, the present study was carried out with the purpose of evaluating the effect of LA on cognitive impairments in scopolamine-induced AD-like rat model.Methods: Forty-two male Wistar rats were divided into six groups to receive normal saline, scopolamine, scopolamine with Donepezil, and scopolamine with varied doses of LA for a period of 21 days. Morris water maze (MWM) and Elevated Plus Maze (EPM) tests were performed to evaluate cognitive performance. After, brains were harvested and processed to assay for the level of malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), acetylcholinesterase (AChE) and interleukin-6 (IL-6). Histological analyses using Haematoxylin and eosin staining was also performed.Results: The LA-treated groups demonstrated memory retention in the MWM and EPM tests, and showed increased levels of CAT, SOD, and GSH similar to the Donepezil group, in contrast to the scopolamine only group while MDA levels, IL-6, and AChE activity were reduced in the LA treated groups contrasted to scopolamine only group. LA reduces oxidative stress, neuroinflammation, and AChE activity, which indicates a possible ability of LA to protect against AD.