Nutritional Neuroscience最新文献

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.

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.

Objectives: Traumatic brain injury (TBI) is severe and may become debilitating for sufferers as a result of damage to the brain. Defining features include primary trauma, axonal damage, as well as both diffuse and focal lesions. One of the many complex biological responses to TBI are neuroinflammation and oxidative stress which are among the most important.

Methods: In this study, we assess the efficacy of polyphenols compounds on managing TBI, given that they are anti-inflammatory and antioxidant. We focus on recent literature that studies the impact of polyphenols on microglial activation as well as balancing the body's inflammatory and oxidative responses.

Results: Evidence demonstrates the ability of polyphenols to lessen the impact of neuroinflammation, oxidative stress, and augmentation of the brain's protective mechanisms and antioxidants. This may help prevent the worsening of brain tissue damage that occurs post TBI. Based on these, there is increasing attention on polyphenols as potential treatment alternatives due to their non-invasive nature.

Discussion: We enumerated some polyphenols with important therapeutic impacts in TBI such as Curcumin and Resveratrol, Quercetin, Gallic acid, Ferulic acid, Luteolin, and Caffeic acid. Their ability to target multiple damaging processes makes them strong candidates.

Objective: This study aimed to assess the effect of safflower oil (SO), a high-quality edible oil derived from seeds of Carthamus tinctorius L. possessing multiple bioactivities, on rats that underwent sciatic nerve crush (SNC) to induce peripheral nerve injury (PNI).

Methods: Sprague-Dawley rats were randomly divided into 4 groups with 10 mice in each group: sham, SNC model, SNC + SO 100 mg/kg, and SNC + SO 300 mg/kg. The sciatic function index (SFI) was monitored for evaluation of sciatic nerve function. Bilateral gastrocnemius muscles were isolated to measure the gastrocnemius muscle mass ratio. Tissue sections of sciatic nerve and gastrocnemius muscle were stained with hematoxylin and eosin for histopathological observations. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, malondialdehyde (MDA), and superoxide dismutase (SOD), and expression of myelin basic protein(MBP) and β₃-tubulin were detected in damaged nerves.

Results: SO supplementation increased the SFI scores, improved the histopathological features of damaged nerves, and enhanced muscle mass and fiber diameters of affected gastrocnemius muscle in SNC rats. SNC-enhanced levels of TNF-α, IL-1β and MDA in damaged nerves were reduced, while SNC-inhibited SOD activity was increased by SO supplementation. Nerve expression of MBP and β₃-tubulin was upregulated in SO-supplemented SNC rats.

Conclusion: Date suggested that SO could improve nerve function, attenuate neuroinflammation and oxidative stress, and might accelerate peripheral nerve regeneration after injury in SNC rats, thus being a promising dietary adjuvant for PNI treatment.

Recent studies have revealed that glaucoma is a neurodegenerative disorder characterized by the degeneration of retinal ganglion cells (RGCs). Neuroinflammation is a significant cause of RGC loss. Vitamin C (Vit C) has been shown to inhibit neuroinflammation in other diseases; however, its effects in glaucoma are yet to be determined. This study aimed to investigate the neuroprotective effects of Vit C on RGCs in glaucoma and the underlying mechanisms. Our findings indicate that Vit C treatment protects against elevated intraocular pressure (IOP)-induced loss of RGCs and thinning of retinal thickness in a chronic ocular hypertension model. Further studies revealed that Vit C reduces the overexpression of glial cells by inhibiting the TLR4/cleaved-caspase-8/NLRP3/cleaved-caspase-1 pathway, thereby alleviating neuroinflammation. Additionally, Vit C was found to inhibit the activation of the Bax/Bcl-2/cleaved-caspase-3 pathway, thus reducing RGC apoptosis. In conclusion, Vit C demonstrates neuroprotective effects in chronic glaucoma, potentially through its roles in reducing neuroinflammation and inhibiting apoptosis, suggesting its therapeutic potential for glaucoma.

Objectives: Olanzapine (Olz) is an effective antipsychotic medication for schizophrenia; however, its use is associated with weight gain and metabolic disorders. Chlorogenic acid (CGA), a dietary polyphenol, has a promising potential for the treatment of obesity, diabetes, and hypertension. This study aimed to determine whether CGA could effectively manage Olz-induced metabolic syndrome (MetS) in a rat model, with metformin (Met) as a positive control.Methods: Female Wistar rats were divided into seven groups: control; Olz (5 mg/kg/day, IP); CGA (20, 40, and 80 mg/kg/day, gavage) plus Olz; Met (100 mg/kg/day, gavage) plus Olz; and CGA (80 mg/kg/day, gavage) for 30 days. Metabolic parameters including body weight, fasting blood glucose, triglycerides, and blood pressure were assessed. This study focused on evaluating serum levels of leptin and adiponectin, as well as hypothalamic protein expression of pro-opiomelanocortin (POMC), neuropeptide Y (NPY), AMP-activated protein kinase (AMPK), and 5-HT2C receptors (5-HT2CR), which are known to influence energy balance and potentially play a role in Olz-induced metabolic abnormalities.Results: Olz caused substantial hyperphagia, weight gain, hypertension, and liver damage, along with elevated fasting blood glucose, triglycerides, and leptin levels. CGA and Met mitigated these effects, although Olz-induced elevation of adiponectin levels remained unaffected by either treatment. Mechanistically, Olz reduced 5-HT2CR protein levels, a trend that was observed in the CGA and Met therapy groups. Olz also enhanced NPY protein levels and the pAMPK/AMPK ratio while lowering POMC protein levels. These alterations were reversed in rats administered CGA or Met.Discussion: These findings suggest that CGA effectively attenuated the adverse metabolic consequences of Olz by modulating leptin, NPY, POMC, and AMPK protein levels. CGA's therapeutic potential highlights its potential as a dietary intervention for managing antipsychotic-induced metabolic disturbances.