Neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis, constitute a major and growing global health burden, with few effective disease-modifying therapies available. Increasing evidence highlights dietary interventions particularly fasting-based regimens as promising non-pharmacological strategies for promoting neuroprotection and cognitive resilience. This review synthesizes current knowledge on the molecular and cellular pathways linking fasting to neuroprotection across neurodegenerative conditions. Fasting can be categorized into intermittent fasting, time-restricted feeding, caloric restriction, and prolonged or periodic fasting. Although these approaches differ in duration and pattern, they share several physiological adaptations. Fasting induces coordinated metabolic, circadian, and gut microbial responses. These responses include a metabolic shift from glucose utilization to ketone body production, realignment of circadian rhythms, and modulation of the gut–brain axis. Collectively, these systemic effects regulate conserved nutrient-sensing and stress-response pathways, including the AMPK–mTOR axis, insulin/IGF-1 signaling, sirtuin-dependent NAD⁺ metabolism, and PGC-1α-mediated mitochondrial biogenesis. At the cellular level, fasting enhances mitochondrial function, maintains redox homeostasis, activates autophagy and proteostasis mechanisms, promotes neurotrophic signaling and synaptic plasticity, and suppresses neuroinflammatory processes. We further integrate preclinical and emerging clinical evidence demonstrating disease-specific benefits of fasting across major NDDs. Finally, translational challenges, safety considerations, and future directions toward personalized fasting strategies and combination therapies are discussed. Collectively, this review underscores fasting as a viable lifestyle-based approach to engage endogenous neuroprotective mechanisms and mitigate neurodegenerative disease progression.
Background Ginger has anti-inflammatory properties, but its effects on ex vivo whole-blood cytokine responses remain unclear. We evaluated ginger supplementation on plasma CRP, immunoglobulins, cortisol, and whole-blood cytokines under basal and stimulated conditions. Design Secondary analysis of a double-blind, 2 × 2 crossover trial in 35 healthy adults randomized to ginger (1500 mg/day) or placebo for 6 weeks, separated by a 4-week washout. Blood was drawn at baseline and the end of each period. Plasma CRP, immunoglobulins, and cortisol were measured. Whole blood was cultured for 24 h unstimulated, with lipopolysaccharide (LPS), or with LPS + phytohemagglutinin (PHA), and cytokines (IFN-γ, IL-4, IL-6, IL-10, IL-17) were quantified. Results A significant treatment × time interaction (p = 0.043) was observed for CRP, with levels decreasing during the ginger period, compared with a slight increase during the placebo period. Basal IL‑10 production decreased within the ginger period (p = 0.047), but the treatment × time interaction was not significant (p = 0.30), indicating no clear between‑treatment difference. LPS-stimulated IL-6 and IL-10 did not differ between treatments. LPS + PHA-stimulated IFN-γ and IL-4 were significantly higher after ginger than placebo (p = 0.014 and p = 0.045, respectively). IL-17 increased within the ginger period (p = 0.049) but the treatment × time interaction was not significant (p = 0.083), so a between‑treatment difference was not supported. Immunoglobulins and cortisol did not change significantly. Conclusions Ginger supplementation produced a modest reduction in systemic CRP, while enhancing mitogen‑driven IFN γ and IL 4 responses. Given the exploratory nature, these findings require confirmation in larger, hypothesis‑driven trials.
Chicken eggs, widely recognized as a nutritional food source, have recently gained attention as a sustainable biomaterial with promising applications in periodontal therapy. Structurally, eggs consist of four main components, such as egg yolk, egg white, eggshell membrane, and eggshell, each possessing distinct physicochemical properties and bioactive compounds that align with key therapeutic goals in periodontal disease management. Emerging pharmacological evidence from preclinical and early clinical studies highlights the multifaceted bioactivities of chicken egg-derived materials, including immunomodulatory, antibacterial, and regenerative effects. Egg yolk-derived immunoglobulin Y demonstrates targeted immune regulation, which interplays with antibacterial activity against periodontopathogens. Egg white fractions exhibit anti-inflammatory properties through inhibition of key signaling pathways, such as NF-κB and MAPK, leading to the downregulation of pro-inflammatory mediators and promotion of anti-inflammatory cytokines, alongside protease inhibitory activity. Meanwhile, eggshell and eggshell membrane are predominantly utilized in surgical approaches, particularly in barrier membranes and grafting applications, due to their osteoconductive properties. This narrative review provides an overview of chicken egg-derived biomaterials as a complementary approach in periodontal therapy to facilitate the evidence-based clinical translation.
In contemporary society, unhealthy dietary patterns increase the risk of intestinal inflammation. Regrettably, intestinal inflammation is also associated with an elevated risk of other inflammatory disorders and metabolic syndrome. Therefore, it is essential to alleviate intestinal inflammation. Natural plant polysaccharides are widely used to alleviate intestinal inflammation owing to their desirable anti-inflammatory properties. In this study, a water-soluble polysaccharide (WSP) is isolated and purified from purple sweet potato (variety of Xuzi 3). The in vivo anti-inflammatory effects of WSP are determined using dextran sulfate sodium (DSS)- and lipopolysaccharide (LPS)-treated mice. From a phenotypic perspective, WSP effectively alleviates DSS and LPS-induced colonic lesions and reduces disease activity index. WSP markedly reduces the levels of ROS, MDA, and pro‑inflammatory cytokines, and increases the activities of antioxidant enzymes in the serum and colonic tissues, thus mitigating oxidative stress and inflammatory response. WSP significantly upregulates the expression of tight junction protein ZO-1 in the colon and further strengthens intestinal physical barrier. At the molecular level, WSP blocks TLR-4/NF-κB and MAPK ERK/JNK signaling cascades. Protein analysis also confirms that WSP does not alleviate endoplasmic reticulum stress in the colon, and WSP promotes mitochondrial fusion and inhibits abnormal mitochondrial fission. In conclusion, WSP improves mitochondrial dynamics and decreases ROS production, which in turn suppresses TLR‑4/NF‑κB and MAPK ERK/JNK pathways and reduces the secretion of pro‑inflammatory cytokines.
Background Cholestasis is a pathological condition characterized by impaired bile synthesis, secretion, or flow, and involves a bidirectional interplay with inflammatory processes. Carrots possess anti-inflammatory properties due to their diverse bioactive compounds. This study evaluated the hepatoprotective potential of Daucus carota seeds essential oil using an in vivo model of cholestasis. Methods Twenty-four adult male Wistar rats (250 ± 20 g) were randomly divided to four groups: (1) control, (2) sham-operated, (3) bile duct ligation (BDL) -induced cholestasis, (4) cholestasis treated with Daucus carota seeds oil at a dose of 2 mg/kg/day for 21 days. Blood and liver samples were collected for serological, gene expression and Immunohistochemical analyses. Results Quantitative analysis of liver histology using ImageJ revealed a significant reduction (p < 0.001) in hepatocyte numbers and an increase in Kupffer cells in the cholestasis group. Enactment with Daucus carota seeds essential oil significantly restored hepatocyte counts and reduced Kupffer cell proliferation. Serological assays demonstrated significant elevations in hepatic biomarkers following cholestasis induction, which were ameliorated by treatment. RT-PCR analysis showed a significant downregulation (p < 0.001) of inflammatory genes, including IL-6, IL-17, TGF-β, TNF-α, and α-SMA, in treated animals compared to the cholestatic group. Additionally, immunohistochemical analysis confirmed elevated TGF-β and α-SMA protein levels in cholestatic livers, which were significantly reduced upon treatment. Conclusions Daucus carota seeds essential oil exerts potent hepatoprotective effects by modulating inflammatory responses and inhibiting the TGF-β/α-SMA signaling pathway. These findings highlight its potential as a natural therapeutic agent for the management of cholestatic liver injury.
