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Therapeutic Opportunities for Food Supplements in Neurodegenerative Disease (2nd Edition)
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Therapeutic Opportunities for Food Supplements in Neurodegenerative Disease (2nd Edition)

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Neuro Sciences".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 3812

Special Issue Editors

Dr. Andrea Domenico Praticò

E-Mail Website
Guest Editor
Unit of Pediatrics, Deparment of Medicine and Surgery, University Kore of Enna, Cittadella Universitaria, 94100 Enna, Italy
Interests: child neurology; neurocutaneous disorders; immune-mediated disease of the central and peripheral nervous system; epilepsy; neurogenetics; movement disorders
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Martino Ruggieri

E-Mail Website
Guest Editor
Unit of Pediatric Clinic, Department of Clinical and Experimental Medicine, University of Catania, 95123 Catania, Italy
Interests: pediatric neurology; neurocutaneous disorders; neurofibromatosis; tuberous sclerosis; Sturge–Weber syndrome; hypomelanosis of Ito; mosaic neurocutaneous disorders; immune-mediated disorders of the nervous system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Numerous epidemiologic studies report a protective association between a balanced and adequate diet and cognitive impairment, brain health and neurodegenerative diseases. At the same time, data from clinical trials supporting these observational findings are also emerging, in particular in childhood and neonatal ages.

These neuroprotective properties may be linked directly to caloric restrictions or to certain neuroprotective properties of food (in long-chain-polyunsaturated fatty acids, vitamin E and mineral elements).

Preventive interventions against neuroinflammation seem to be able to interfere with neurodegeneration, enhance the antioxidative defense and lower the risk and incidence of age-related diseases, such as cardiovascular and neurodegenerative diseases. It should be noted that dietary-supplementation-based strategies have been demonstrated to be effective in subjects with mild cognitive impairment, or directly in metabolic disorders in which a specific enzymatic deficit may require targeted dietary restrictions. 

In some studies, adjunctive supplementation has also been demonstrated to improve depression, which is a marked benefit considering the comorbidity between cognitive impairment/dementia and depression.

Dr. Andrea Domenico Praticò
Prof. Dr. Martino Ruggieri
Guest Editors

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurological disorders
  • neurodegenerative disorders
  • diet
  • food
  • free radicals
  • anti-oxidants

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Published Papers (3 papers)

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Research

26 pages, 9348 KB  
Article
Dietary Yam (Dioscorea opposita Thunb.) Ameliorates Parkinson’s Disease in Mice via Gut Microbiota-Driven Mitochondrial Improvement and Neuroinflammation Inhibition
by Shuqing Zhang, Wenjia Pan, Chen Ma, Yinghua Luo, Li Dong, Junfu Ji, Lingjun Ma, Daotong Li and Fang Chen
Nutrients 2026, 18(8), 1208; https://doi.org/10.3390/nu18081208 - 11 Apr 2026
Viewed by 366
Abstract
Background/Objectives: Parkinson’s disease (PD) is a progressive neurodegenerative disorder that poses a substantial threat to global human health. Yam (Dioscorea opposita Thunb.) is a traditional medicinal and edible plant that has long been used in Asia, Africa, and the Caribbean. Its major [...] Read more.
Background/Objectives: Parkinson’s disease (PD) is a progressive neurodegenerative disorder that poses a substantial threat to global human health. Yam (Dioscorea opposita Thunb.) is a traditional medicinal and edible plant that has long been used in Asia, Africa, and the Caribbean. Its major bioactive components, such as dioscin and polysaccharides, have been reported to exhibit neuroprotective effects; however, the impact of dietary yam on PD progression remains to be elucidated. Therefore, we sought to evaluate its neuroprotective potential and the underlying mechanisms in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP)-induced PD mice. Methods: Mice received six-week dietary yam supplementation. Behavioral, histological, and neurochemical analyses were performed to assess motor function, dopaminergic neuron integrity, and dopamine levels. Gut microbiota and metabolic profiles were analyzed using 16S rRNA gene sequencing and non-targeted metabolomics. Transcriptomic sequencing and Western blot analysis of the substantia nigra pars compacta (SNc) were conducted to investigate molecular mechanisms, and integrative multi-omics analysis was applied to explore microbiota–metabolite–host interactions. Results: Yam supplementation improved motor function, preserved nigrostriatal dopaminergic neurons, and restored striatal dopamine levels in PD mice. Notably, yam was associated with the maintenance of intestinal homeostasis by strengthening barrier integrity and enriching beneficial taxa, including Ileibacterium, Lachnospiraceae NK4A136 group, and Blautia. Consistently, yam also elevated neuroprotective purines and amino acids, including inosine, xanthine, and succinic acid. At the molecular level, yam treatment modulated mitochondrial oxidative phosphorylation by increasing PGC-1α and COX7c expression, and reduced inflammasome-related neuroinflammatory signaling. Integrative modeling showed significant associations between yam-modulated genes and PD-related indices with microbiota and metabolites. Conclusions: These findings suggest that yam may represent a potential dietary strategy for alleviating PD-related neurodegeneration by modulating the microbiota–gut–brain axis. Full article
(This article belongs to the Special Issue Therapeutic Opportunities for Food Supplements in Neurodegenerative Disease (2nd Edition))
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18 pages, 2736 KB  
Article
Phycocyanobilin as a Functional Food-Derived Nutraceutical Candidate for Modulating the RAGE/NOX4 Axis in Neurodegenerative Disorders
by Mei Chou Lai, Yu-Cheng Tzeng, Wayne Young Liu and I-Min Liu
Nutrients 2026, 18(4), 617; https://doi.org/10.3390/nu18040617 - 13 Feb 2026
Viewed by 557
Abstract
Background/Objectives: Neurodegeneration associated with diabetes and metabolic dysfunction involves interconnected processes, including advanced glycation end product (AGE)-related signaling, RAGE/NOX4-dependent oxidative stress, dysregulated endoplasmic reticulum (ER) stress, and mitochondrial apoptosis. Phycocyanobilin (PCB), a tetrapyrrolic chromophore of C-phycocyanin, has been proposed to exert pleiotropic [...] Read more.
Background/Objectives: Neurodegeneration associated with diabetes and metabolic dysfunction involves interconnected processes, including advanced glycation end product (AGE)-related signaling, RAGE/NOX4-dependent oxidative stress, dysregulated endoplasmic reticulum (ER) stress, and mitochondrial apoptosis. Phycocyanobilin (PCB), a tetrapyrrolic chromophore of C-phycocyanin, has been proposed to exert pleiotropic cytoprotective effects; however, its actions within glycation-associated neuronal stress pathways remain incompletely defined. Methods: Differentiated SH-SY5Y neurons were exposed to AGEs (300 μg/mL) for a 24 h period to examine whether PCB modulates neuronal injury along the RAGE–NOX4–oxidative-stress–ER-stress–mitochondrial axis. The selective RAGE antagonist TTP488 (100 μmol/L) was included as a pharmacological reference. Neuronal viability, neurite integrity, intracellular and mitochondrial reactive oxygen species, ER stress signaling, and apoptotic markers were assessed using complementary biochemical, molecular, and functional assays. Results: PCB pretreatment (10–50 μmol/L) significantly improved neuronal viability, preserved neurite structure, and reduced oxidative stress under the AGE challenge. These effects were accompanied by attenuation of AGEs-induced upregulation of RAGE and NOX4 expression, suppression of PERK–eIF2α–ATF4–CHOP signaling, restoration of mitochondrial apoptotic balance, inhibition of caspase activation, and reduced DNA fragmentation. The overall protective profile of PCB was comparable to that observed with TTP488 at the level of downstream pathway modulation. Conclusions: These findings suggest that PCB mitigates glycation-associated neuronal injury through coordinated regulation of oxidative, ER stress, and mitochondrial apoptotic pathways linked to RAGE/NOX4 signaling, supporting further investigation of PCB as a functional food-derived bioactive in metabolic stress-related neurodegeneration. Full article
(This article belongs to the Special Issue Therapeutic Opportunities for Food Supplements in Neurodegenerative Disease (2nd Edition))
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14 pages, 255 KB  
Article
Sapropterin Dihydrochloride Responsiveness in Phenylketonuria: A Case Series Exploring Gaps in Comprehensive Patient Monitoring
by Manuela Lo Bianco, Roberta Leonardi, Alessia Migliore, Evelina Moliteo, Monica Sciacca, Sergio Rinella, Maria Grazia Pappalardo, Luisa La Spina, Marianna Messina, Riccardo Iacobacci, Martino Ruggieri, Concetta Meli and Agata Polizzi
Nutrients 2025, 17(17), 2892; https://doi.org/10.3390/nu17172892 - 7 Sep 2025
Viewed by 2210
Abstract
Background: Phenylketonuria (PKU) is a rare autosomal recessive metabolic disorder caused by mutations in the phenylalanine hydroxylase (PAH) gene, leading to hyperphenylalaninemia (HPA). Untreated, elevated phenylalanine (Phe) levels cause severe neurocognitive, developmental, and psychiatric complications. Management relies on a Phe-restricted [...] Read more.
Background: Phenylketonuria (PKU) is a rare autosomal recessive metabolic disorder caused by mutations in the phenylalanine hydroxylase (PAH) gene, leading to hyperphenylalaninemia (HPA). Untreated, elevated phenylalanine (Phe) levels cause severe neurocognitive, developmental, and psychiatric complications. Management relies on a Phe-restricted diet, which is challenging to maintain, particularly in adolescents and adults. Sapropterin dihydrochloride, a synthetic form of tetrahydrobiopterin (BH4), can enhance residual PAH activity, lowering blood Phe levels and increasing dietary tolerance in responsive patients. However, real-world alignment with best practices remains underexplored. This study aims to report a tertiary referral center’s experience with sapropterin treatment in PKU and assess adherence to international guidelines. Methods: We retrospectively analyzed 23 PKU patients treated with sapropterin from 2007 to 2025. Patients with baseline Phe levels of 360–2000 µmol/L underwent a 10 mg/kg/day loading test over two weeks. Responsiveness was defined as a ≥30% reduction in blood Phe levels. Phe levels were measured pre- and post-test, and dietary tolerance was evaluated. Adherence to best practices was critically reviewed. Results: All patients showed significant Phe reductions (mean 71.43%, p < 0.0001), exceeding responsiveness thresholds. Most achieved substantial increases in dietary Phe tolerance, with three patients partially responsive (800–1200 mg/day). Responsiveness was unrespectful of the patient’s genotype, for those individuals for whom this was known (8/23 patients). Although effective, the test dose and duration differed from guideline recommendations (20 mg/kg/day). Neuropsychological and QoL assessments were not systematically performed, representing a key limitation. Conclusions: Sapropterin dihydrochloride effectively identified responders and improved dietary flexibility even with lower dosing protocols. Greater adherence to international standards, particularly regarding long-term neuropsychological monitoring, is needed to optimize patient care. Full article
(This article belongs to the Special Issue Therapeutic Opportunities for Food Supplements in Neurodegenerative Disease (2nd Edition))
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