Nutritional Neuroscience最新文献

Objectives: Alzheimer's disease (AD) is a neurodegenerative disease characterized by cognitive impairment. This situation imposes a great burden on individuals, both economically and socially. Today, an effective method for treating the disease and protective approach to tau accumulation has not been developed yet. Studies have been conducted on the effects of hesperidin and naringin flavonoids found in citrus fruits on many diseases.

Methods: In this review, the pathophysiology of AD is defined, and the effects of hesperidin and naringin on these factors are summarized.

Results: Studies have shown that both components may potentially affect AD due to their antioxidative and anti-inflammatory properties. Based on these effects of the components, it has been shown that they may have ameliorative effects on Aβ, α-synuclein aggregation, tau pathology, and cognitive functions in the pathophysiology of AD.

Discussion: There are studies suggesting that hesperidin and naringin may be effective in the prevention/treatment of AD. When these studies are examined, it is seen that more studies should be conducted on the subject.

Background: Medium-chain fatty acids (MCFAs) and docosahexaenoic acid (DHA) could affect the occurrence of mild cognitive impairment (MCI). β-hydroxybutyrate (BHB), mitochondrial DNA copy number (mtDNAcn) and mitochondrial DNA (mtDNA) deletions might be their potential mechanisms. This study aimed to explore the relationship between MCFAs, DHA and MCI, and potential mechanisms.

Methods: This study used data from Tianjin Elderly Nutrition and Cognition (TENC) cohort study, 120 individuals were identified with new onset MCI during follow-up, 120 individuals without MCI were selected by 1:1 matching sex, age, and education levels as the control group from TENC. Conditional logistic regression analysis and mediation effect analysis were used to explore their relationship.

Results: Higher serum octanoic acid levels (OR: 0.633, 95% CI: 0.520, 0.769), higher serum DHA levels (OR: 0.962, 95% CI: 0.942, 0.981), and more mtDNAcn (OR: 0.436, 95% CI: 0.240, 0.794) were associated with lower MCI risk, while more mtDNA deletions was associated with higher MCI risk (OR: 8.833, 95% CI: 3.909, 19.960). Mediation analysis suggested that BHB and mtDNAcn, in series, have mediation roles in the association between octanoic acid and MCI risk, and mtDNA deletions have mediation roles in the association between DHA and MCI risk.

Conclusion: Higher serum octanoic acid and DHA levels were associated with lower MCI risk. Octanoic acid could affect the incidence of MCI through BHB, then mitochondria function, or through mitochondria function, or directly. Serum DHA level could affect the incidence of MCI through mitochondria function, or directly.

Protein deficiency, characterized by an inadequate intake of protein in the diet that fails to meet the body's physiological requirements across various stages, can lead to detrimental outcomes. This is of interest due to the persistent low protein content in staple foods and suboptimal dietary patterns. The study sought to assess the intergenerational repercussions of dietary protein deficiency on specific neurochemicals and the cytoarchitecture of the brain within the F1 and F2 generations of rats. The rats were categorized into four groups based on the protein content percentage in their diets: 21% protein diet (21%PD), 10% protein diet (10%PD), 5% protein diet (5%PD), and control diet. Neurobehavior was assessed, while brain serotonin and dopamine levels were measured using HPLC. BDNF and GDNF expression in the hippocampal and prefrontal (PFC) sections, Immunohistochemical investigations of the morphological impact on the hippocampus and PFC, were also analyzed. The protein-deficient groups displayed anxiety, loss of striatal serotonin and increased dopamine levels, degenerated pyramidal cells in the hippocampus, and a prominent reduction in cellular density in the PFC. BDNF and GDNF levels in the PFC were reduced in the 5%PD group. GFAP astrocyte expression was observed to be increased in the prefrontal cortex (PFC) and hippocampal sections, indicating heightened reactivity. The density of hypertrophied cells across generations further suggests the presence of neuroinflammation. Changes in brain structure, neurotransmitter levels, and neurotrophic factor levels may indicate intergenerational alterations in critical regions, potentially serving as indicators of the brain's adaptive response to address protein deficiency across successive generations.

Many epidemiological studies have shown the beneficial effects of a largely plant-based diet, and the strong association between the consumption of a Mediterranean-type diet with healthy aging including a lower risk of cognitive decline. The Mediterranean diet is characterized by a high intake of olive oil, fruits and vegetables and is rich in dietary fiber and polyphenols - both of which have been postulated to act as important mediators of these benefits. Polyphenols are large molecules produced by plants to protect them from environmental threats and injury. When ingested by humans, as little as 5% of these molecules are absorbed in the small intestine with the majority metabolized by the gut microbiota into absorbable simple phenolic compounds. Flavan-3-ols, a type of flavonoid, contained in grapes, berries, pome fruits, tea, and cocoa have been associated with many beneficial effects on several risk factors for cardiovascular disease, cognitive function and brain regions involved in memory formation. Both preclinical and clinical studies suggest that these brain and heart benefits can be attributed to endothelial vascular effects and anti-inflammatory properties among others. More recently the gut microbiota has emerged as a potential modulator of the aging brain and intriguingly polyphenols have been shown to alter microbiota composition and be metabolized by different microbial species. However, there is a need for well controlled studies in large populations to identify predictors of response, particularly given the vast inter-individual variation of human gut microbiota.

Objective: Ischemic stroke is the leading cause of mortality and disability worldwide with more than half of survivors living with serious neurological sequelae thus, it has recently attracted considerable attention in the field of medical research. Neurogenesis is the process of formation of new neurons in the brain, including the human brain, from neural stem/progenitor cells [NS/PCs] which reside in neurogenic niches that contain the necessary substances for NS/PC proliferation, differentiation, migration, and maturation into functioning neurons which can integrate into a pre-existing neural network.Neurogenesis can be modulated by many exogenous and endogenous factors, pathological conditions. Both brain-derived neurotrophic factor, and flavonoids can modulate the neurogenic process in physiological conditions and after various pathological conditions including ischemic insults.

Aim: This review aims to discuss neurogenesis after ischemic insults and to determine the role of flavonoids and BDNF on neurogenesis under physiological and pathological conditions with a concentration on ischemic insults to the brain in particular.

Method: Relevant articles assessing the impact of flavonoids and BDNF on neurogenic processes in various physiological/pathological conditions including ischemic insults within the timeline of 1965 until 2023 were searched using the PubMed database.

Conclusions: The selected studies have shown that ischemic insults to the brain induce NS/PC proliferation, differentiation, migration, and maturation into functioning neurons integrating into a pre-existing neural network. Flavonoids and BDNF can modulate neurogenesis in the brain in various physiological/pathological conditions including ischemic insults. In conclusion, flavonoids and BDNF may be involved in post-ischemic brain repair processes through enhancing endogenous neurogenesis.

Diet can regulate systemic inflammation, which may play an important role in the development and progression of cognitive impairment and dementia. To explore the relationship between the dietary inflammatory potential and cognitive ability. A total of 2307 adults aged 60 years or older were recruited from the Fujian Provincial Hospital (Fujian, China). Dietary inflammatory properties were analyzed using the energy-adjusted dietary inflammatory index (E-DII). The Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) were used to assess cognitive function. Logistic regression and restricted cubic spline (RCS) were fit to assess the associations between variables. The MCI subjects with the highest E-DII scores had a higher risk of AD compared to subjects with the lowest E-DII scores (OR = 1.98, 95%CI = 1.49-2.64, P for trend < 0.001). Subjects with the highest E-DII levels were at increased risk of cognitive impairment compared to those with the lowest E-DII levels (OR = 1.56, 95%CI = 1.25-1.93, P for trend < 0.001). The link between E-DII and cognitive impairment was significant in a nonlinear dose response analysis (P for nonlinear = 0.001). Higher E-DII scores were associated with an increased risk of developing AD or cognitive impairment. These findings may contribute to the effective prevention of cognitive impairment by constructing a multidisciplinary synergistic prevention strategy and controlling dietary inflammation levels.

Background: To comprehensively assess the neurologic recovery potential of chondroitinase ABC (ChABC) in rats after spinal cord injury (SCI).

Methods: The PubMed, Embase, ScienceDirect, Web of Science, and China National Knowledge Infrastructure databases were searched for animal experiments that evaluated the use of ChABC in the treatment of SCI up to November 2022. Studies reporting neurological function using the Basso, Beattie, and Bresnahan (BBB) scale, as well as assessments of cavity area, lesion area, and glial fibrillary acidic protein (GFAP) levels, were included in the analysis.

Results: A total of 46 studies were ultimately selected for inclusion. The results of the study showed that rats with SCI that received ChABC therapy exhibited a significant improvement in locomotor function after 7 days compared with controls (32 studies, weighted mean difference (WMD) = 0.58, [0.33, 0.83], p < 0.00001). Furthermore, the benefits of ChABC therapy were maintained for up to 28 days according to BBB scale. The lesion area was reduced by ChABC (5 studies, WMD = -20.94, [-28.42, -13.46], p < 0.00001). Meanwhile, GFAP levels were reduced in the ChABC treatment group (8 studies, WMD = -29.15, [-41.57, -16.72], p < 0.00001). Cavity area is not statistically significant. The subgroup analysis recommended that a single injection of 10 μL (8 studies, WMD = 2.82, [1.99, 3.65], p < 0.00001) or 20 U/mL (4 studies, WMD = 2.21, [0.73, 3.70], p = 0.003) had a better effect on improving the function. The funnel plot of the BBB scale was found to be essentially symmetrical, indicating a low risk of publication bias.

Conclusions: This systematic review and meta-analysis has indicated that ChABC could improve functional recovery in rats after SCI.

Objective: The Manihot esculenta Crantz (Cassava) is a typical South American plant rich in nutrients and energetic compounds. Lately, our group has shown that non-pharmacological interventions with natural antioxidants present different neuroprotective effects on oxidative balance and memory deficits in AD-like animal models. Here, our objective was to evaluate the neuroprotective effects of Cassava leaves' extract (CAS) in an AD-like model induced by amyloid-beta (Aβ) 25-35 peptide.

Methods: Male Wistar rats (n = 40; 60 days old) were subjected to 10 days of CAS supplementation; then, we injected 2 μL Aβ 25-35 in the hippocampus by stereotaxic surgery. Ten days later, we evaluated object recognition (OR) memory. Cassavas' total polyphenols, flavonoids, and condensed tannins content were measured, as well as hippocampal lipid peroxidation and total antioxidant capacity.

Results: CAS protected against Aβ-induced OR memory deficits. In addition, Aβ promoted antioxidant capacity decrease, while CAS was able to prevent it, in addition to diminishing lipoperoxidation compared to Aβ.

Discussion: We show that treatment with Cassava leaves' extract before AD induction prevents recognition memory deficits related to Aβ hippocampal injection. At least part of these effects can be related to the Cassava leaves' extract supplementation effects on diminishing lipid peroxidation and preventing a decrease in the hippocampal total antioxidant capacity in the hippocampus of AD-like animals without adverse effects. Once cassavais a plant of warm and dry ground that can adapt to growon various soil types and seems to resist several insects, our results enable Cassava to be considered asa potential preventive intervention to avoid or minimizeAD-induced memory deficits worldwide.

Objective: This study aimed to assess the association between vitamin D and sleep health and to investigate whether depression could mediate this relationship.

Methods: A cross-sectional analysis was performed using the 2005-2014 US National Health and Nutrition Examination Survey (NHANES) data. The logistic regression models were conducted to evaluate association of serum vitamin D concentrations with sleep health and depression. Mediation analyses were conducted to investigate the mediated effects of depression on the association of vitamin D with sleep health.

Results: In multivariate logistic models, vitamin D was found to be negatively associated with an increased risk of poor sleep health, with an odds ratio (OR) of vitamin D deficiency versus sufficiency was 1.256 (95% CI = 1.084-1.455). Additionally, univariate logistic models showed that vitamin D was also negatively associated with depression risk (vitamin D deficiency vs. sufficiency: OR = 1.699, 95% CI = (1.373-2.103). Further mediation analyses showed that the association of vitamin D with sleep health was mediated by depression, with the mediating effects of depression accounted for 44.56% of the total effects.

Conclusion: Vitamin D affects sleep health directly and indirectly through depression. The results suggest that interventions increasing intake of vitamin D should be prioritized to promote sleep health of persons with or at risk of depression.

Background: The effect of an intervention based on Mediterranean diet on reducing recurrence risk or subsyndromal depressive symptoms in recovered depressed patients has not been explored.

Methods: The PREDIDEP study was a two-year randomized trial designed to assess the effect of the Mediterranean Diet enriched with extra virgin olive oil on depression recurrence. At baseline and at four, eight, 16, 20, and 24 months of follow-up, depressive symptoms were evaluated through the Beck Depression inventory. Cox regression analysis was fitted to assess the role of dietary intervention on the risk of depression recurrence. Mixed effects linear models were used to assess changes in depressive subsyndromal symptoms according to the intervention.

Results: After two years of intervention, the dietary intervention group (n = 103) compared to the control group (n = 93) showed no differences regarding depression recurrence risk as main outcome. As secondary outcomes, an improvement of depressive symptoms was yielded at four (-2.15; 95% CI = -4.00 to -0.29) and eight months (-2.42; 95% CI = -4.17 to -0.67) in the intervention group, with no changes in control group. Moreover, at 20 months, significant differences were found between groups (-3.35; 95% CI = -6.08 to -0.61).

Conclusions: An intervention with Mediterranean diet in patients with previous depressive episodes might contribute to the reduction of depressive subsyndromal symptoms.