Nutritional Neuroscience最新文献

Objectives: This study aimed to assess the contribution of edible/cooking oils and mayonnaise sauce in the severity, motor and non-motor symptoms, and risk of Parkinson's disease (PD).Methods: In this study, 120 patients with PD and 50 healthy individuals participated. The frequency and quantity of edible/cooking oils including animal and plant source oils (hydrogenated and nonhydrogenated) and mayonnaise sauce used by participants were determined using a food frequency questionnaire. The severity of PD was determined by the Unified Parkinson's Disease Rating Scale (UPDRS).Results: Patients with PD had lower use of hydrogenated plant-based oil (HPO) (p < 0.001) and animal oils (p < 0.001) but had higher use of non-hydrogenated plant-based oil (NHPO) (p < 0.001), olive oil (p = 0.02), and mayonnaise sauce (p < 0.001) compared with the healthy subjects. Use of each unit HPO reduced 4% the odds of PD (p = 0.01). The odds of PD increased 20% by each unit increase in NHPO usage (p = 0.001), 49% by olive oil (p = 0.02), and 127% by mayonnaise sauce (p = 0.004) intake. According to receiver operator characteristics curve analysis, mayonnaise sauce and NHPO had the largest area under the curve in predicting PD. Intake of animal oil was positively correlated with total score of UPDRS (p = 0.05) and motor symptoms (p = 0.04). Intake of butter was positively correlated with total score of UPDRS (p = 0.047), nonmotor aspects of experiences of daily living (p = 0.02), and motor examination (p = 0.02).Discussion: The findings indicate that high intake of HPO reduces, while high intake of NHPO, olive oil, and mayonnaise sauce increases the odds of PD.

Objectives: Animal studies have indicated that fat intake mediates amygdala activation, which in turn promotes fat intake, while amygdala activation increases the preference for fat and leads to increased fat intake. However, the association among fat intake, amygdala activation, and appetite for high-calorie foods in humans remains unclear. Thus, to examine this association, we conducted a functional magnetic resonance imaging (fMRI) experiment.

Methods: Fifty healthy-weight adults (18 females; mean age: 22.9 ± 3.02 years) were included. Participants were shown images of high-calorie and low-calorie foods and were instructed to rate their desire to eat the food items during fMRI. All participants provided information on their daily fat intake using a self-reported questionnaire. Associations among fat intake, the desire to eat high-calorie or low-calorie food items, and amygdala responses to food items were examined.

Results: The basolateral amygdala (BLA) response was positively associated with fat intake ([x, y, z] = [24, -6, -16], z = 3.91, p_{FWE-corrected} = 0.007) and the desire to eat high-calorie food items ([26, -4, -16], z = 3.75, p_{FWE-corrected} = 0.010). Structural equation modeling showed that the desire for high-calorie food items was predicted by BLA response to high-calorie food items (p = 0.013, β = 3.176), and BLA response was predicted by fat intake (p < 0.001, β = 0.026).

Discussion: Fat intake influences BLA response to high-fat food, which in turn increases the desire to eat palatable high-fat food. This may lead to additional fat intake and increase the risk of weight gain.

Objectives: Epilepsy is a chronic neurological condition with recurrent seizures. One-third of epilepsy patients experience unacceptable side effects from antiepileptic drugs. Pyrus pashia is a deciduous tree from southern Asia. Ethnomedicinally, Malakand tribes use its fruits for epilepsy treatment. Our prior research demonstrated the anticonvulsive properties of ethanolic extract of Pyrus pashia (EPP) and its bioactive compound chrysin in acute seizure tests. This study aims to investigate the impact of EPP and chrysin on cognitive impairment in a PTZ-induced kindling mice model of epilepsy.

Methods: Swiss albino male mice were equally divided into four groups. The first group received 0.5% carboxy methyl cellulose dissolved in normal saline while the other three groups were pre-treated with Diazepam (DZP) (1 mg/kg, i.p.), EPP (200 mg/kg, p.o.) and chrysin (5 mg/kg, p.o.). After 30 min, all groups were administered PTZ (35 mg/kg, i.p.) and evaluated for seizure severity, cognitive function, and neuronal apoptosis. Western blot analysis was conducted to analyze the expressions of apoptosis biomarkers and memory-related genes, including cAMP response element-binding protein (CREB) and Brain Derived Neurotrophic Factor (BDNF).

Results: The therapeutic effects of EPP and Chrysin were comparable to DZP in terms of reducing seizure severity, but unlike DZP, they prevented PTZ-induced memory impairment in experimental animals. Additionally, they increased the levels of BDNF and CREB while reducing apoptotic biomarkers in the hippocampus of experimental animals.

Conclusions: Based on the leads offered by this study EPP and its major bioactive constituent, could be developed as the treatment option for epilepsy.

Objective: Prenatal protein malnutrition produces anatomical and functional changes in the developing brain that persist despite immediate postnatal nutritional rehabilitation. Brain networks of prenatally malnourished animals show diminished activation of prefrontal areas and an increased activation of hippocampal regions during an attentional task [1]. While a reduction in cell number has been documented in hippocampal subfield CA1, nothing is known about changes in neuron numbers in the prefrontal or parahippocampal cortices.

Methods: In the present study, we used unbiased stereology to investigate the effect of prenatal protein malnutrition on the neuron numbers in the medial prefrontal cortex and the cortices of the parahippocampal region that comprise the larger functional network.

Results: Results show that prenatal protein malnutrition does not cause changes in the neuronal population in the medial prefrontal cortex of adult rats, indicating that the decrease in functional activation during attentional tasks is not due to a reduction in the number of neurons. Results also show that prenatal protein malnutrition is associated with a reduction in neuron numbers in specific parahippocampal subregions: the medial entorhinal cortex and presubiculum.

Discussion: The affected regions along with CA1 comprise a tightly interconnected circuit, suggesting that prenatal malnutrition confers a vulnerability to specific hippocampal circuits. These findings are consistent with the idea that prenatal protein malnutrition produces a reorganization of structural and functional networks, which may underlie observed alterations in attentional processes and capabilities.

Background: Idiopathic intracranial hypertension (IIH) is a disorder that primarily affects obese women of reproductive age. The exact pathogenesis of IIH is unknown though multiple etiologies have been proposed.

Case presentation: We report a case of IIH triggered by first-time Ramadan intermittent fasting (RIF) in an 18-year-old woman. Our patient developed new onset headaches, diplopia, and pulsatile tinnitus with examination notable for bilateral papilledema and lumbar puncture revealing an elevated opening pressure. Her symptoms resolved after cessation of RIF, apart from persistent left sided tinnitus which later resolved with acetazolamide administration.

Conclusion: This case report uniquely illustrates that RIF may provoke symptomatic IIH. We hypothesize that a decreased concentration of glucagon-like peptide-1 (GLP-1) induced by fasting results in decreased GLP-1 receptor activation in the choroid plexus, allowing for increased CSF secretion into the ventricles invoking increased intracranial pressure (ICP). This theoretical mechanism provides further insight as to the possible underlying pathophysiology of IIH.

Context: Spinal cord injury (SCI) is a potentially fatal neurological disease with severe complications and a high disability rate. An increasing number of animal experimental studies support the therapeutic effect of quercetin, which is a natural anti-inflammatory and antioxidant bioflavonoid.

Objective: This paper reviewed the therapeutic effect of quercetin on a rat SCI model and summarized the relevant mechanistic research.

Data sources: PubMed, EMBASE, Web of Science, Science Direct, WanFang Data, SinoMed databases, the China National Knowledge Infrastructure, and the Vip Journal Integration Platform were searched from their inception to April 2023 for animal experiments applying quercetin to treat SCI.

Study selection: Based on the PICOS criteria, a total of 18 eligible studies were included, of which 14 were high quality.

Results: In this study, there was a gradual increase in effect based on the Basso, Beattie, and Bresnahan (BBB) score after three days (p < 0.0001). Furthermore, gender differences also appeared in the efficacy of quercetin; males performed better than females (p = 0.008). Quercetin was also associated with improved inclined plane test score (p = 0.008). In terms of biochemical indicators, meta-analysis showed that MDA (p < 0.0001) and MPO (p = 0.0002) were significantly reduced after quercetin administration compared with the control group, and SOD levels were increased (p = 0.004). Mechanistically, quercetin facilitates the inhibition of oxidative stress, inflammation, autophagy and apoptosis that occur after SCI.

Conclusions: Generally, this systematic review suggests that quercetin has a neuroprotective effect on SCI.

Parkinson's disease (PD) is a chronic neurodegenerative disease (NDD) due to the degeneration of dopaminergic neurons (DNs) in the substantia nigra (SN). PD is characterized by diverse motor symptoms such as rigidity, resting tremors, and bradykinesia, and non-motor symptoms such as cognitive dysfunction and sleep disturbances. Vitamin D (VD), VD receptor (VDR), and VD metabolites are present in the brain and play a role in maintaining the development, differentiation, and functions of the DNs. VDRs exert protective effects against PD neuropathology by modulating functional capacity and DNs neurotransmission in the SN. In virtue of its anti-inflammatory and antioxidant activities, VD could be effective in the prevention and treatment of PD. VD exerts a neuroprotective effect by reducing oxidative stress and mitochondrial dysfunction, and by increasing autophagy and brain-derived neurotrophic factor (BDNF). Low VD serum level is connected with cognitive dysfunction and the development of dementia in PD. The VD-mediated cognitive augmenting effect is interrelated to the safeguarding of synaptic plasticity and modulation of neurotransmitter release. VD deficiency is linked with the severity of olfactory dysfunction which precedes the progression of symptomatic PD. However, the precise role of VD in PD remains unidentified, and there is a conflict about whether treatment with VD can ameliorate PD or not.

ABSTRACTKetamine, an N-methyl-D-aspartate receptor antagonist, produces rapid antidepressant effects in patients with treatment-resistant depression. However, owing to the undesirable adverse effects of ketamine, there is an urgent need for developing safer and more effective prophylactic and therapeutic interventions for depression. Preclinical studies have demonstrated that activation of the mechanistic target of rapamycin complex 1 (mTORC1) in the medial prefrontal cortex (mPFC) mediates the rapid antidepressant effects of ketamine. The steroidal alkaloid tomatidine and its glycoside α-tomatine (tomatine) can activate mTORC1 signaling in peripheral tissues/cells. We examined whether tomatidine and tomatine exerted prophylactic and therapeutic antidepressant-like actions via mPFC mTORC1 activation using a mouse model of lipopolysaccharide (LPS)-induced depression. Male mice were intraperitoneally (i.p.) administered tomatidine/tomatine before and after the LPS challenge to test their prophylactic and therapeutic effects, respectively. LPS-induced depression-like behaviors in the tail suspension test (TST) and forced swim test (FST) were significantly reversed by prophylactic and therapeutic tomatidine/tomatine administration. LPS-induced anhedonia in the female urine sniffing test was reversed by prophylactic, but not therapeutic, injection of tomatidine, and by prophylactic and therapeutic administration of tomatine. Intra-mPFC infusion of rapamycin, an mTORC1 inhibitor, blocked the prophylactic and therapeutic antidepressant-like effects of tomatidine/tomatine in TST and FST. Moreover, both tomatidine and tomatine produced antidepressant-like effects in ovariectomized female mice, a model of menopause-associated depression. These results indicate that tomatidine and tomatine exert prophylactic and therapeutic antidepressant-like effects via mTORC1 activation in the mPFC and suggest these compounds as promising candidates for novel prophylactic and therapeutic agents for depression.

Trehalose is a naturally occurring sugar found in various food and pharmaceutical preparations with the ability to enhance cellular proteostasis and reduce the formation of toxic intracellular protein aggregates, making it a promising therapeutic candidate for various neurodegenerative disorders.

Objectives: Here, we explored the effectiveness of nutritional trehalose supplementation in ameliorating symptoms in a mouse model of Fragile X-associated tremor/ataxia syndrome (FXTAS), an incurable late onset manifestation of moderately expanded trinucleotide CGG repeat expansion mutations in the 5' untranslated region of the fragile X messenger ribonucleoprotein 1 gene (FMR1).

Methods: An inducible mouse model of FXTAS expressing 90 CGG repeats in the brain had been previously developed, which faithfully captures hallmarks of the disorder, the formation of intracellular inclusions, and the disturbance of motor function. Taking advantage of the inducible nature of the model, we investigated the therapeutic potential of orally administered trehalose under two regimens, modelling disease prevention and disease treatment.

Results and discussion: Trehalose's effectiveness in combating protein aggregation is frequently attributed to its ability to induce autophagy. Accordingly, trehalose supplementation under the prevention regimen ameliorated the formation of intranuclear inclusions and improved the motor deficiencies resulting from the induced expression of 90 CGG repeats, but it failed to reverse the existing nuclear pathology as a treatment strategy. Given the favorable safety profile of trehalose, it is promising to further explore the potential of this agent for early stage FXTAS.

Introduction: Autism spectrum disorders (ASDs) are a group of neurodevelopmental disorders with poor social interaction, communication issues, aberrant motor movements, and limited repetitive interests and behaviour. Spirulina platensis (SP) contains several multi-nutrients and has a wide range of neuroprotective properties.Aim: The target of the current experiment is to detect the protective effects of S. platensis on valproic-induced autism in adult female albino rats' siblings for the first time.Materials and Methods: Twelve Pregnant rats were separated into four main groups; Group I (control); Group II (S. platensis); Group III (autistic group); and Group IV (autistic SP-treated group). Fifteen offspring pups from each group were sacrificed, brain was divided for biochemical analysis as superoxide dismutase and malondialdehyde were evaluated spectrophotometrically while interleukin-6, interleukin-12, Bcl-2-associated X protein, B-cell lymphoma-2, Beclin-1, brain-derived neurotrophic factor were assessed by ELISA, other division of brain were used for gene expression of PI3k, Akt and mTOR pathway, last division of brain were stained using (H&E) and Giemsa stains. Tumour necrosis factor alpha (TNF-$\alpha )$ and Synaptophysin (SYN) markers were used for immunohistochemical staining.Results: Autistic Group (III) showed an increment in levels of MDA, IL-6, IL12 and BAX while showing a decrement in SOD, Bcl-2 and Beclin-1 as well as increased PI3k, Akt and mTOR gene expression. Autistic Group (III) also exhibited hypocellularity and disorganization of hippocampal and prefrontal cortex cells. The autistic SP-treated group (IV) showed improvement in these biochemical markers and pathological changes. Our findings suggest that Spirulina platensis will be significant in managing autism.