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Brain Sciences
Special Issues
Metabolic Alterations in Neurodegenerative Diseases and Treatment Options
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Metabolic Alterations in Neurodegenerative Diseases and Treatment Options

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neurodegenerative Diseases".

Deadline for manuscript submissions: closed (15 July 2023) | Viewed by 5803

Special Issue Editors

Dr. Sandeep Singh

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Guest Editor
Indian Scientific Education and Technology (ISET) Foundation, Lucknow 226002, India
Interests: neuroscience; Alzheimer's disease; natural products; therapeutic; drug discovery; oxidative stress; nutraceuticals
Special Issues, Collections and Topics in MDPI journals
Dr. Soraya L. Valles

E-Mail Website
Guest Editor
Department of Physiology, University of Valencia, 46010 València, Spain
Interests: neuroscience; neuroinflammation; Alzheimer's disease; ELA
Special Issues, Collections and Topics in MDPI journals
Dr. Burkhard Poeggeler

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Guest Editor
Department of Physiology, Johann-Friedrich-Blumenbach-Institute for Zoology and Anthropology, Faculty of Biology Georg August University Göttingen, Göttingen and Goettingen Research Campus, Göttingen, Am Türmchen 3, D-33332 Gütersloh, Germany
Interests: aging; amino acids; antioxidants; inflammaging; melatonin; product development; tryptophan
Special Issues, Collections and Topics in MDPI journals
Dr. Anastasiia D. Shkodina

E-Mail Website
Guest Editor Assistant
Department of Neurological Diseases with Neurosurgery and Medical Genetics, Poltava State Medical University, Poltava, Ukraine
Interests: neurodegenerative diseases; psychiatric syndromes; circadian misalignment

Special Issue Information

Dear Colleagues,

Metabolic and energetic disturbances have recently been considered not only as a consequence, but also as one of the causes of neurodegeneration. A well-known attribute of neurodegenerative diseases, such as in Alzheimer's disease, Parkinson's disease and others, is the progressive loss of neurons. Despite the fact that the causes of these diseases can be polyetiological, they have a wide range of similar molecular and cellular pathophysiological processes, namely protein aggregation, glutamate toxicity, calcium, proteolytic and oxidative stress, neuroinflammation, mitochondrial dysfunction, hormonal changes and others, associated with aging.

Neurodegenerative diseases are age dependent, so their development is closely related to common aging mechanisms and metabolic lesions. Cell cultures, animal models, and human studies show close connection between neurodegeneration and metabolic alterations, namely, obesity, glucose metabolism disturbances, and impairments in hormone secretion, including melatonin, leptin, ghrelin, etc. Although many have known about the pathogenesis of neurodegenerative diseases, they still do not have a therapy capable of stopping the progression and modern methods are directed at the symptoms of the disease.

This Special Issue aims to highlight the numerous metabolic changes in neurodegenerative diseases and related current therapeutic approaches.

Dr. Sandeep Singh
Prof. Dr. Soraya L. Valles
Dr. Burkhard Poeggeler
Dr. Anastasiia D. Shkodina
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 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

  • Parkinson’s disease
  • Alzheimer’s disease
  • metabolism
  • metabolites
  • hormones
  • inflammation
  • neurodegeneration
  • drug discovery
  • therapy

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Published Papers (2 papers)

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Research

14 pages, 2542 KiB  
Article
The Impact of Some Modulators of the Renin–Angiotensin System on the Scopolamine-Induced Memory Loss Mice Model
by Daniela-Carmen Ababei, Ioana-Miruna Balmus, Walther Bild, Alin Stelian Ciobica, Radu Marian Lefter, Răzvan-Nicolae Rusu, Gabriela Dumitrita Stanciu, Sabina Cojocaru, Monica Hancianu and Veronica Bild
Brain Sci. 2023, 13(8), 1211; https://doi.org/10.3390/brainsci13081211 - 16 Aug 2023
Viewed by 1555
Abstract
As some of the renin–angiotensin–aldosterone system (RAAS)-dependent mechanisms underlying the cognitive performance modulation could include oxidative balance alterations, in this study we aimed to describe some of the potential interactions between RAAS modulators (Losartan and Ramipril) and oxidative stress in a typical model [...] Read more.
As some of the renin–angiotensin–aldosterone system (RAAS)-dependent mechanisms underlying the cognitive performance modulation could include oxidative balance alterations, in this study we aimed to describe some of the potential interactions between RAAS modulators (Losartan and Ramipril) and oxidative stress in a typical model of memory impairment. In this study, 48 white male Swiss mice were divided into six groups and received RAAS modulators (oral administration Ramipril 4 mg/kg, Losartan 20 mg/kg) and a muscarinic receptors inhibitor (intraperitoneal injection scopolamine, 0.5 mg/kg) for 8 consecutive days. Then, 24 h after the last administration, the animals were euthanized and whole blood and brain tissues were collected. Biological samples were then processed, and biochemical analysis was carried out to assess superoxide dismutase and glutathione activities and malondialdehyde concentrations. In the present experimental conditions, we showed that RAAS modulation via the angiotensin-converting enzyme inhibition (Ramipril) and via the angiotensin II receptor blockage (Losartan) chronic treatments could lead to oxidative stress modulation in a non-selective muscarinic receptors blocker (scopolamine) animal model. Our results showed that Losartan could exhibit a significant systemic antioxidant potential partly preventing the negative oxidative effects of scopolamine and a brain antioxidant potential, mainly by inhibiting the oxidative-stress-mediated cellular damage and apoptosis. Ramipril could also minimize the oxidative-mediated damage to the lipid components of brain tissue resulting from scopolamine administration. Both blood serum and brain changes in oxidative stress status were observed following 8-day treatments with Ramipril, Losartan, scopolamine, and combinations. While the serum oxidative stress modulation observed in this study could suggest the potential effect of RAAS modulation and scopolamine administration on the circulatory system, blood vessels endothelia, and arterial tension modulation, the observed brain tissues oxidative stress modulation could lead to important information on the complex interaction between renin–angiotensin and cholinergic systems. Full article
(This article belongs to the Special Issue Metabolic Alterations in Neurodegenerative Diseases and Treatment Options)
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25 pages, 5548 KiB  
Article
Olive- and Coconut-Oil-Enriched Diets Decreased Secondary Bile Acids and Regulated Metabolic and Transcriptomic Markers of Brain Injury in the Frontal Cortexes of NAFLD Pigs
by Magdalena A. Maj, Tanvi R. Gehani, Chad Immoos, Mikaelah S. Medrano, Rob K. Fanter, Christine R. Strand, Hunter Glanz, Brian D. Piccolo, Mohammed K. Abo-Ismail, Michael R. La Frano and Rodrigo Manjarín
Brain Sci. 2022, 12(9), 1193; https://doi.org/10.3390/brainsci12091193 - 4 Sep 2022
Cited by 5 | Viewed by 2755
Abstract
The objective of this study was to investigate the effect of dietary fatty acid (FA) saturation and carbon chain length on brain bile acid (BA) metabolism and neuronal number in a pig model of pediatric NAFLD. Thirty 20-day-old Iberian pigs, pair-housed in pens, [...] Read more.
The objective of this study was to investigate the effect of dietary fatty acid (FA) saturation and carbon chain length on brain bile acid (BA) metabolism and neuronal number in a pig model of pediatric NAFLD. Thirty 20-day-old Iberian pigs, pair-housed in pens, were randomly assigned to receive one of three hypercaloric diets for 10 weeks: (1) lard-enriched (LAR; n = 5 pens), (2) olive-oil-enriched (OLI, n = 5), and (3) coconut-oil-enriched (COC; n = 5). Pig behavior and activity were analyzed throughout the study. All animals were euthanized on week 10 and frontal cortex (FC) samples were collected for immunohistochemistry, metabolomic, and transcriptomic analyses. Data were analyzed by multivariate and univariate statistics. No differences were observed in relative brain weight, neuronal number, or cognitive functioning between diets. Pig activity and FC levels of neuroprotective secondary BAs and betaine decreased in the COC and OLI groups compared with LAR, and paralleled the severity of NAFLD. In addition, OLI-fed pigs showed downregulation of genes involved in neurotransmission, synaptic transmission, and nervous tissue development. Similarly, COC-fed pigs showed upregulation of neurogenesis and myelin repair genes, which caused the accumulation of medium-chain acylcarnitines in brain tissue. In conclusion, our results indicate that secondary BA levels in the FCs of NAFLD pigs are affected by dietary FA composition and are associated with metabolic and transcriptomic markers of brain injury. Dietary interventions that aim to replace saturated FAs by medium-chain or monounsaturated FAs in high-fat hypercaloric diets may have a negative effect on brain health in NAFLD patients. Full article
(This article belongs to the Special Issue Metabolic Alterations in Neurodegenerative Diseases and Treatment Options)
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