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Nutrients and Neurodegenerative Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (10 May 2023) | Viewed by 17886

Special Issue Editors


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Guest Editor
Department of Biology, Unit of General Physiology, University of Pisa, 56126 Pisa, Italy
Interests: human physiology; neurobiology; neurodegeneration

Special Issue Information

Dear Colleagues,

At present, it is increasingly evident that a correct diet is essential for maintaining the state of brain health. Macronutrient and micronutrient deficiency and metabolic disorders of lipid, carbohydrate and protein metabolism have been involved in the pathogenetic mechanisms of neurodegenerative disorders. Different specific nutrients are considered essential for the prevention and/or treatment of Parkinson disease, Alzheimer disease, multiple sclerosis and others. This Special Issue welcomes the submission of original research papers or comprehensive reviews that demonstrate or summarize significant advances in the field of nutrients in the pathogenesis and/or treatment of different neurodegenerative disorders.

Prof. Dr. Elisabetta Albi
Dr. Maria de las Mercedes Garcia-Gil
Guest Editors

Manuscript Submission Information

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Keywords

  • lipids
  • vitamins
  • minerals
  • carbohydrates
  • proteins
  • neurodegenerative diseases

Published Papers (5 papers)

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Research

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18 pages, 7952 KiB  
Article
Effects of Nutraceuticals on Cisplatin-Induced Cytotoxicity in HEI-OC1 Cells
by Lorenzo Guidotti, Elena Tomassi, Silvia Marracci, Michele Lai, Dominga Lapi, Rossana Pesi, Laura Pucci, Ettore Novellino, Elisabetta Albi and Mercedes Garcia-Gil
Int. J. Mol. Sci. 2023, 24(24), 17416; https://doi.org/10.3390/ijms242417416 - 12 Dec 2023
Viewed by 1416
Abstract
Cisplatin is a chemotherapeutic drug for the treatment of several solid tumors, whose use is limited by its nephrotoxicity, neurotoxicity, ototoxicity, and development of resistance. The toxicity is caused by DNA cross-linking, increase in reactive oxygen species and/or depletion of cell antioxidant defenses. [...] Read more.
Cisplatin is a chemotherapeutic drug for the treatment of several solid tumors, whose use is limited by its nephrotoxicity, neurotoxicity, ototoxicity, and development of resistance. The toxicity is caused by DNA cross-linking, increase in reactive oxygen species and/or depletion of cell antioxidant defenses. The aim of the work was to study the effect of antioxidant compounds (Lisosan G, Taurisolo®) or hydrogen sulfide (H2S)-releasing compounds (erucin) in the auditory HEI-OC1 cell line treated with cisplatin. Cell viability was determined using the MTT assay. Caspase and sphingomyelinase activities were measured by fluorometric and colorimetric methods, respectively. Expression of transcription factors, apoptosis hallmarks and genes codifying for antioxidant response proteins were measured by Western blot and/or RT-qPCR. Lisosan G, Taurisolo® and erucin did not show protective effects. Sodium hydrosulfide (NaHS), a donor of H2S, increased the viability of cisplatin-treated cells and the transcription of heme oxygenase 1, superoxide dismutase 2, NAD(P)H quinone dehydrogenase type 1 and the catalytic subunit of glutamate-cysteine ligase and decreased reactive oxygen species (ROS), the Bax/Bcl2 ratio, caspase-3, caspase-8 and acid sphingomyelinase activity. Therefore, NaHS might counteract the cytotoxic effect of cisplatin by increasing the antioxidant response and by reducing ROS levels and caspase and acid sphingomyelinase activity. Full article
(This article belongs to the Special Issue Nutrients and Neurodegenerative Diseases)
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19 pages, 2814 KiB  
Article
The Masticatory Activity Interference in Quantitative Estimation of CA1, CA3 and Dentate Gyrus Hippocampal Astrocytes of Aged Murine Models and under Environmental Stimulation
by Marília da Cunha Feio Leal, Fabio Leite do Amaral Junior, Bernardo Freire da Silva Arruda, Juliana Ayumi Azevedo Kurosawa, Amanda Almeida Vieira, Júlia Corrêa Campos Maia, Viviana Virgínia Bezerra Scalfoni, Antonio Morais da Silveira Junior, Matheus Oliveira Feijó, Fernanda Beatriz Araújo de Albuquerque, Maria Helena Moutinho Marta, Marina Paula Nobre Normando, Alana Gabriele Oliveira Cabeça da Silva, Fernanda Catharina Pires da Trindade, Fabíola de Carvalho Chaves de Siqueira Mendes and Marcia Consentino Kronka Sosthenes
Int. J. Mol. Sci. 2023, 24(7), 6529; https://doi.org/10.3390/ijms24076529 - 31 Mar 2023
Cited by 2 | Viewed by 1916
Abstract
Studies indicating the influence of masticatory dysfunction, due to a soft diet or lack of molars, on impairing spatial memory and learning have led to research about neuronal connections between areas and cell populations possibly affected. In this sense, with scarce detailed data [...] Read more.
Studies indicating the influence of masticatory dysfunction, due to a soft diet or lack of molars, on impairing spatial memory and learning have led to research about neuronal connections between areas and cell populations possibly affected. In this sense, with scarce detailed data on the subfields of hippocampus in dementia neurodegeneration, there is no information about astrocytic responses in its different layers. Thus, considering this context, the present study evaluated the effects of deprivation and rehabilitation of masticatory activity, aging, and environmental enrichment on the stereological quantification of hippocampal astrocytes from layers CA1, CA3, and DG. For this purpose, we examined mature (6-month-old; 6M), and aged (18-month-old; 18M) mice, subjected to distinct masticatory regimens and environments. Three different regimens of masticatory activity were applied: continuous normal mastication with hard pellets (HD); normal mastication followed by deprived mastication with equal periods of pellets followed by soft powder (HD/SD); or rehabilitated masticatory activity with equal periods of HD, followed by powder, followed by pellets (HD/SD/HD). Under each specific regimen, half of the animals were raised in standard cages (impoverished environment (IE)) and the other half in enriched cages (enriched environment (EE)), mimicking sedentary or active lifestyles. Microscopic stereological, systematic, and random sampling approaches with an optical dissector of GFAP-immunolabeled astrocytes were done, allowing for an astrocyte numerical estimate. Stratum moleculare and hilus, from the dentate gyrus (DG) and Strata Lacunosum-Moleculare, Oriens, and Radiatum, similarly to the dentate gyrus, showed no significant change in any of the investigated variables (age, diet, or environment) in these layers. However, in Stratum radiatum, it was possible to observe significant differences associated with diet regimens and age. Therefore, diet-related differences were found when the HD 18M IE group was compared to the HD/SD/HD 18-month-old group in the same environment (IE) (p = 0.007). In the present study, we present modulatory factors (masticatory function, environmental enrichment, and aging) for the differentiated quantitative laminar response in the hippocampal regions, suggesting other studies to read the plasticity and responsiveness of astrocytes, including the molecular background. Full article
(This article belongs to the Special Issue Nutrients and Neurodegenerative Diseases)
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18 pages, 3065 KiB  
Article
The Polyunsaturated Fatty Acid EPA, but Not DHA, Enhances Neurotrophic Factor Expression through Epigenetic Mechanisms and Protects against Parkinsonian Neuronal Cell Death
by Maria Rachele Ceccarini, Veronica Ceccarelli, Michela Codini, Katia Fettucciari, Mario Calvitti, Samuela Cataldi, Elisabetta Albi, Alba Vecchini and Tommaso Beccari
Int. J. Mol. Sci. 2022, 23(24), 16176; https://doi.org/10.3390/ijms232416176 - 19 Dec 2022
Cited by 4 | Viewed by 2534
Abstract
ω-3 Polyunsaturated fatty acids (PUFAs) have been found to exert many actions, including neuroprotective effects. In this regard, the exact molecular mechanisms are not well understood. Parkinson’s disease (PD) is the second most common age-related neurodegenerative disease. Emerging evidence supports the hypothesis that [...] Read more.
ω-3 Polyunsaturated fatty acids (PUFAs) have been found to exert many actions, including neuroprotective effects. In this regard, the exact molecular mechanisms are not well understood. Parkinson’s disease (PD) is the second most common age-related neurodegenerative disease. Emerging evidence supports the hypothesis that PD is the result of complex interactions between genetic abnormalities, environmental toxins, mitochondrial dysfunction, and other cellular processes, such as DNA methylation. In this context, BDNF (brain-derived neurotrophic factor) and GDNF (glial cell line-derived neurotrophic factor) have a pivotal role because they are both involved in neuron differentiation, survival, and synaptogenesis. In this study, we aimed to elucidate the potential role of two PUFAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and their effects on BDNF and GDNF expression in the SH-SY5Y cell line. Cell viability was determined using the MTT assay, and flow cytometry analysis was used to verify the level of apoptosis. Transmission electron microscopy was performed to observe the cell ultrastructure and mitochondria morphology. BDNF and GDNF protein levels and mRNA were assayed by Western blotting and RT-PCR, respectively. Finally, methylated and hydroxymethylated DNA immunoprecipitation were performed in the BDNF and GDNF promoter regions. EPA, but not DHA, is able (i) to reduce the neurotoxic effect of neurotoxin 6-hydroxydopamine (6-OHDA) in vitro, (ii) to re-establish mitochondrial function, and (iii) to increase BNDF and GDNF expression via epigenetic mechanisms. Full article
(This article belongs to the Special Issue Nutrients and Neurodegenerative Diseases)
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Review

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21 pages, 1614 KiB  
Review
Microglia and Brain Disorders: The Role of Vitamin D and Its Receptor
by Alessandra Mirarchi, Elisabetta Albi, Tommaso Beccari and Cataldo Arcuri
Int. J. Mol. Sci. 2023, 24(15), 11892; https://doi.org/10.3390/ijms241511892 - 25 Jul 2023
Cited by 2 | Viewed by 2293
Abstract
Accounting for 5–20% of the total glial cells present in the adult brain, microglia are involved in several functions: maintenance of the neural environment, response to injury and repair, immunesurveillance, cytokine secretion, regulation of phagocytosis, synaptic pruning, and sculpting postnatal neural circuits. Microglia [...] Read more.
Accounting for 5–20% of the total glial cells present in the adult brain, microglia are involved in several functions: maintenance of the neural environment, response to injury and repair, immunesurveillance, cytokine secretion, regulation of phagocytosis, synaptic pruning, and sculpting postnatal neural circuits. Microglia contribute to some neurodevelopmental disorders, such as Nasu–Hakola disease (NHD), Tourette syndrome (TS), autism spectrum disorder (ASD), and schizophrenia. Moreover, microglial involvement in neurodegenerative diseases, such as Alzheimer’s (AD) and Parkinson’s (PD) diseases, has also been well established. During the last two decades, epidemiological and research studies have demonstrated the involvement of vitamin D3 (VD3) in the brain’s pathophysiology. VD3 is a fat-soluble metabolite that is required for the proper regulation of many of the body’s systems, as well as for normal human growth and development, and shows neurotrophic and neuroprotective actions and influences on neurotransmission and synaptic plasticity, playing a role in various neurological diseases. In order to better understand the exact mechanisms behind the diverse actions of VD3 in the brain, a large number of studies have been performed on isolated cells or tissues of the central nervous system (CNS). Here, we discuss the involvement of VD3 and microglia on neurodegeneration- and aging-related diseases. Full article
(This article belongs to the Special Issue Nutrients and Neurodegenerative Diseases)
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18 pages, 950 KiB  
Review
Effect of a Vegan Diet on Alzheimer’s Disease
by Alzbeta Katonova, Katerina Sheardova, Jana Amlerova, Francesco Angelucci and Jakub Hort
Int. J. Mol. Sci. 2022, 23(23), 14924; https://doi.org/10.3390/ijms232314924 - 29 Nov 2022
Cited by 10 | Viewed by 8836
Abstract
There is evidence indicating that a vegan diet could be beneficial in the prevention of neurodegenerative disorders, including Alzheimer’s disease (AD). The purpose of this review is to summarize the current knowledge on the positive and negative aspects of a vegan diet regarding [...] Read more.
There is evidence indicating that a vegan diet could be beneficial in the prevention of neurodegenerative disorders, including Alzheimer’s disease (AD). The purpose of this review is to summarize the current knowledge on the positive and negative aspects of a vegan diet regarding the risk of AD. Regarding AD prevention, a vegan diet includes low levels of saturated fats and cholesterol, contributing to a healthy blood lipid profile. Furthermore, it is rich in phytonutrients, such as vitamins, antioxidants, and dietary fiber, that may help prevent cognitive decline. Moreover, a vegan diet contributes to the assumption of quercetin, a natural inhibitor of monoamine oxidase (MAO), which can contribute to maintaining mental health and reducing AD risk. Nonetheless, the data available do not allow an assessment of whether strict veganism is beneficial for AD prevention compared with vegetarianism or other diets. A vegan diet lacks specific vitamins and micronutrients and may result in nutritional deficiencies. Vegans not supplementing micronutrients are more prone to vitamin B12, vitamin D, and DHA deficiencies, which have been linked to AD. Thus, an evaluation of the net effect of a vegan diet on AD prevention and/or progression should be ascertained by taking into account all the positive and negative effects described here. Full article
(This article belongs to the Special Issue Nutrients and Neurodegenerative Diseases)
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