This study aimed to investigate the effects of Mediterranean and Western diet models on telomere length, oxidative stress, inflammatory markers, and total hippocampal cell count in rats. Twenty-one male Sprague - Dawley rats (8 weeks old) were randomly assigned to Control, Mediterranean, and Western diet groups (n = 7 per group). Following an eight-week specific dietary intervention, telomere lengths were measured by PCR, biochemical parameters (oxidative stress and inflammation) by ELISA and colorimetric methods, and hippocampal cell counts using the isotropic fractionator. The Western diet group exhibited significantly higher body weight and BMI compared to other groups (p < 0.05). Telomere length was significantly longer in the Mediterranean diet group compared to the Western diet group (p < 0.05). Regarding inflammatory markers, TNF- α levels were significantly higher, whereas IL- 10 levels were significantly lower in the Western diet group compared to the Mediterranean group. Additionally, hippocampal cell counts were significantly reduced in the Western diet group. Dietary intake of omega- 3 and resveratrol was positively associated with telomere length. The Mediterranean diet appears to protect telomere integrity and hippocampal cell survival by mitigating oxidative stress and inflammation. Conversely, the Western diet accelerates molecular aging markers. These findings highlight the translational potential of dietary composition in modulating cellular senescence.

ABSTRACT Objectives: Cerebrovascular function declines with normal ageing, and the antioxidant and anti-inflammatory properties of Vitamin E may maintain or improve this. The aim of this systematic review is to evaluate the effect of vitamin E on cerebrovascular function in both pre-clinical and clinical populations. Methods: Six databases (PubMed, MEDLINE, Web of Science, Scopus, ScienceDirect, and CINAHL) were searched in 2024 using keywords such as ‘vitamin E’, tocopherol, tocotrienol, ‘cerebrovascular function’, and related medical subject heading terms. Results: Of the 335 records returned, no clinical studies were identified. Ten pre-clinical studies met the inclusion criteria and were included for analysis. Due to heterogeneity in study designs and outcomes, a meta-analysis was not performed. Across animal models of cerebral ischaemia and haemorrhagic hypoperfusion, vitamin E supplementation improved cerebral blood flow, reduced intracranial pressure, and enhanced cerebrovascular responsiveness, thus reflecting improved cerebrovascular function. Furthermore, studies examining platelet aggregation reported delayed thrombus formation, likely mediated by reduced oxidative stress and improved endothelial function and nitric oxide bioavailability. However, with heterogeneous outcomes from pre-clinical studies and a lack of clinical studies, the translatability of data to the effect of chronic consumption on cerebrovascular function in humans is limited. Discussion: Pre-clinical data suggest that the antioxidant capacity of vitamin E and its regulatory effect on platelet aggregation may improve cerebrovascular function. However, the absence of clinical data limits translation to human populations. Future well-designed studies in older adults are warranted to determine whether vitamin E supplementation can preserve or improve cerebrovascular function throughout the ageing process.

ABSTRACT Introduction: Current treatments for Alzheimer’s disease (AD) are primarily supportive and have limited efficacy in slowing disease progression. Therefore, the search for new therapeutic agents is essential to improve cognitive deficits or potentially prevent the advancement of this neurodegenerative disorder. Baru oil (BO) contains several bioactive compounds that may possess neuroprotective effects. However, no studies have investigated the potential beneficial effects of BO in the context of AD. Aim and Methods: This study aimed to investigate the neuroprotective effects of BO in a rodent model of AD. Mice were pretreated orally with vehicle or BO 1 or 3 g/kg/day for 45 days. On the 30th day, mice were infused i.c.v with amyloid-beta (Aβ) or PBS. A positive control group was orally treated with memantine (20mg/kg/day) for 15 days after Aβ or PBS infusion. Following behavioral assessments, mice were euthanized and the brains were removed for biochemical assays. Results: Similar to memantine treatment, pretreatment with both doses of BO prevented Aβ-induced memory impairments in the Morris water maze and the object recognition task. Pretreatment with BO 3g/kg/day prevented Aβ-induced increase in lipid peroxidation in the hippocampus. BO pretreatment mitigated the Aβ-induced reductions in hippocampal expression levels of BDNF, TrkB, and p-CREB. BO prevented the Aβ-induced increase in COX-2 and NOS-2 expression in the hippocampus. Conclusion: BO reversed Aβ-induced cognitive deficits. These neuroprotective effects were associated with the mitigation of hippocampal oxidative stress and neuroinflammation, alongside the restoration of the BDNF/TrkB/p-CREB signaling pathway. Our findings highlight Baru oil as a promising multifactorial therapeutic agent for AD.

ABSTRACT Background Evening chronotype has been linked with depression and dietary behaviour. However, the mechanism that links circadian preference to diet quality in university students remains unclear. Psychological distress may mediate this pathway among university students prone to social jet lag. Objective The present study investigates whether psychological distress mediates the association between chronotype and diet quality associations in university students, and to explore gender specific patterns. Methods A cross-sectional study was conducted among 238 university students in Haryana, India (mean age-21.1 ± 3.15 years). The participants completed measures, including the Diet Quality Questionnaire (DQQ), the Morningness-Eveningness Scale, and the Depression, Anxiety, and Stress Scale-21 (DASS-21). The Generalised Linear Modelling with 1000 bootstrapped resamples to estimate the indirect and direct effects of chronotype on diet quality via stress, anxiety, and depression, with confidence intervals including gender-stratified analysis. Results The findings report that evening chronotype was significantly associated with depression (β = −0.118, p = 0.031) at the component level, with the chronotype depression link being stronger in females, but directly associated with poor diet quality (β = 0.0828, p = 0.063). However, the indirect pathway was not significant, and all the bootstrapped confidence intervals for indirect effects had crossed zero in the total sample and by gender. The model explained 3.2% of the variance in diet quality. Conclusion The study results indicate that sleep quality, together with light exposure, which the researchers did not measure in the research process, provides a better explanation for how chronotype affects students’ dietary habits. The future studies should incorporate objective measures of sleep and daily light exposure.

ABSTRACT Objectives: Prebiotics may reduce adiposity and inflammation, improving cognitive function in obese rats, mediated by modulation of the gut–brain axis. Banana-based snacks are promising prebiotic foods. However, their effects on gut microbiota, inflammation, brain reactive oxygen species (ROS) production, microglial morphology, dendritic spine density, and cognitive function remain underexplored in high-fat diet (HFD)-induced obese rats. Methods: Seventy-two male rats were maintained on either a normal diet (ND) or a HFD for 16-weeks. At week 13, ND-fed rats were subdivided into six groups (n = 6/group) receiving either a vehicle (NDV, 10.5 mL/kg/day twice daily), prebiotic snacks from bananas at ripening stages 2–5 (NDS2-5, 7.47 g in water, 10.5 mL/kg/day twice daily), or inulin (NDI, 2 g/kg/day in water, 10.5 mL/kg/day twice daily). HFD-fed rats were similarly subdivided into six groups (n = 6/group) with either a vehicle (HFV), banana-based prebiotic snacks (HFS2-5), or inulin (HFI), administered for four weeks at the same doses as the ND-fed rats. Results: HFD-fed rats exhibited both obesity and insulin resistance, gut dysbiosis, inflammation, and cognitive impairment. However, rats receiving inulin or banana-based prebiotics from all ripening stages exhibited improved cognitive function by reducing gut dysbiosis, oxidative stress, inflammation, brain ROS, apoptosis, dendritic spine loss, and microglial activation. Conclusions: Prebiotic banana snacks from all ripening stages may protect against HFD-induced cognitive impairment by enhancing gut health and reducing inflammation and oxidative stress, potentially via the gut-brain axis. These findings support their potential use as functional foods to promote both cognitive and metabolic health.

ABSTRACT Objective To investigate the synergistic effects of combined human milk oligosaccharides (HMOs) and lactoferrin (Lf) supplementation on brain metabolites and neurotransmitters in neonatal piglets using proton magnetic resonance spectroscopy (¹H-MRS). Methods Three-day-old male domestic piglets were randomly assigned to three groups and fed for 35 days with a standard pig milk replacer supplemented as follows: control (methylcellulose, 1.8 g/L; n = 14), combined HMOs (cHMOs, 70% 2′-FL and 30% 3′-SL:6′-SL in a 1:2.5 ratio, 1.8 g/L; n = 16), or cHMOs + Lf (cHMOs, 1.8 g/L + Lf, 0.5 g/L; n = 14). In vivo ¹H-MRS was performed on postnatal day 38–39 using a 3 T scanner (TE = 30 ms) to assess regional brain metabolite profiles. Results The combined cHMOs and Lf group exhibited significantly higher absolute levels of total lipids and macromolecules (tLM), along with increased relative concentrations of glutathione (GSH), total creatine (tCr), total choline (tCho), and tLM (p < 0.05). The cHMOs alone group showed a similar upward trend in tCr, tCho, and tLM, but exhibited significantly higher absolute levels of total N-acetylaspartate (tNAA) (p < 0.05) compared with the other two groups. Collectively, these findings indicate distinct metabolic profiles among the treatment groups. Conclusions The combined cHMOs and Lf supplementation may synergistically support neurodevelopment by enhancing lipid mobilization, energy metabolism, and antioxidant capacity, while cHMOs alone promotes brain development by improving neuronal integrity and synaptic activity in piglets – a translational model for human infants. To our knowledge, these findings have not been previously reported.

ABSTRACT Background Sleep is essential for infant health and cognitive development. Poor sleep increases the risk of childhood obesity and weakens immune health. Infant sleep is a major concern for parents, as disruptions can impact parental sleep and overall well-being, leading to various negative consequences. Prebiotic foods introduced during the complementary feeding period may potentially improve infant sleep and, consequently, parental sleep. However, to our knowledge, no studies have yet explored this relationship. Methods As a secondary outcome analysis of a three-arm parallel randomized control trial (ACTRN12620000026921), this paper compared the effects of kūmara (K group, n = 93) or kūmara with added resistant starch (K+ group, n = 93) to a control group (n = 95) on infant sleep and caregiver sleep quality during the first four months of complementary feeding. Infant and caregiver sleep were subjectively assessed at baseline (prior to solids), and at two (Complementary Feeding 2, CF2) and four (Complementary Feeding 4, CF4) months post-introduction to solids, using the caregiver-reported Brief Infant Sleep Questionnaire (BISQ) and Patient-Reported Outcomes Measurement Information System (PROMIS®) scales for Sleep Disturbance and Sleep-Related Impairment, respectively. Results Compared to the control group, infants in the K group had significantly less nocturnal wakefulness (8.4 min, p = 0.023) at CF4. The K+ group showed a near-significant increase in daytime sleep (11.4 min, p = 0.053) but also trends toward more reports of problematic nighttime sleep at CF2. Caregiver sleep outcomes did not differ significantly. Discussion Kūmara consumption may reduce nocturnal wakefulness in infants, but further research incorporating objective sleep measures and exploring underlying mechanisms is needed. Trial registration Australian New Zealand Clinical Trials Registry identifier: ACTRN12620000026921.

ABSTRACT Introduction Multiple sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system with a high prevalence of dysphagia (43.3%), increasing the risk of aspiration pneumonia, malnutrition and dehydration. Objectives This study aimed to (i) describe the sociodemographic and anthropometric characteristics of adults with MS; (ii) estimate the risk of dysphagia and evaluate speech and oropharyngeal impairments in relation to this risk and (iii) examine dietary patterns and nutritional status indicators according to the presence or absence of dysphagia risk. Methodology An observational, cross-sectional and analytical study was conducted in 52 patients with MS from Granada. Body composition was assessed by multifrequency bioelectrical impedance analysis (NUTRILAB). Dietary intake was recorded using three 24-hour recalls and a food frequency questionnaire (FFQ). Data were processed using Dietowin software. The speech and language-therapy assessment included the Yale Swallow Protocol, TOMASS and a taste perception protocol. Results 57.7% of participants were at risk of dysphagia. ‘Double texture alert’ and ‘salivation alteration’ were significantly more frequent in the at-risk group. No significant differences were found between participants with and without dysphagia risk in anthropometric measures – excepting FFM and BMR – or nutrient intake. However, 61.5% of the sample showed excess body weight and altered intake of macro- and micronutrients. Moreover, more than 50% of participants exhibited inadequacies in consumption habits across most food groups. Conclusions A high prevalence of dysphagia risk was observed. Patients at risk tended to show higher BMI, inadequate intake and taste alterations. These findings highlight the need for early screening and interdisciplinary, individualised nutritional and speech therapy interventions.

ABSTRACT Mild cognitive impairment occurring with age is an intermediate stage between normal cognitive functioning and dementia. Precisely, because of the lack of unequivocal symptoms, the deterioration of cognitive functions that occurs with age is a growing concern for the aging population. Therefore, the aim of this study was to verify the prophylactic potential of genistein (5,7-dihydroxy-3-(4-hydroxyphenyl)-4H-1-benzopyran-4-one) in preventing memory loss of healthy individuals. The experiments were conducted using wild-type mice of both sexes that were not genetically modified. Analysis of cognitive processes in genistein-supplemented and untreated animals was carried out using behavioral tests (elevated plus maze, novel object recognition, and Morris water maze tests). In addition, microscopic assessment of the number of amyloid beta deposits in key brain structures for memory processes was performed. Our results suggest that genistein has a potential in preventing the impairment of memory processes resulting from aging. This proposal is supported not only by the results of behavioral tests, but also by microscopic analyses showing a reduction in the number of beta-amyloid aggregates in the brain after genistein supplementation.

ABSTRACT Background and Objectives Stress in day-to-day life affects the body system differently by altering homeostasis and biological processes. The foremost sign of chronic stress-induced disorders is reflected in behavioral activity. Chronic stress affects the brain negatively, it modulates neurobehavioral activity and impairs the associated activities like learning, memory, and cognition. Emerging evidence suggests that virgin coconut oil (VCO), is an abundant source of natural antioxidants with anti-inflammatory, antidepressant, and neuroprotective potential. However, VCO's efficacy in ameliorating chronic restraint stress-induced abnormal changes is rarely understood. Hence, we aimed to evaluate VCO's neuroprotective potential in attenuating chronic restraint stress-induced neurobehavioral and biochemical alteration in rats. Methods A total of eighteen male Wistar rats were allocated into three groups (n = 6/group): Control (C) – saline (5 ml/kg/21 days), Stress (S) – restraint stress (6hrs/day/21 days), and Test (S + VCO) (6 hrs/day+5 ml/kg VCO for 21 days). The behavioral (Radial arm maze (RAM)) and biochemical (corticosterone (CORT)), reduced glutathione (GSH), and malonaldehyde (MDA) parameters were analyzed to determine the neuroprotective effect of VCO. Results The VCO-treated group has shown a significant increase in the percentage of correct choice entries and a reduction in error entries, highlighting an improvement in working and reference memory. Moreover, there was a substantial elevation in GSH, and a reduction in MDA and CORT levels, indicating a potent antioxidant activity of VCO. Additionally, significant body weight gain and reduced adrenal gland weight were noted in VCO-treated rats. Conclusions Our findings signify that VCO has therapeutic potential to improve spatial learning memory and antioxidant status in chronic restraint stress rats. Schematic depiction of the protective effect of virgin coconut oil on chronic restraint stress rats.