Special Issue "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: 15 July 2023 | Viewed by 1926

Special Issue Editors

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
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

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

Published Papers (1 paper)

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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
Brain Sci. 2022, 12(9), 1193; https://doi.org/10.3390/brainsci12091193 - 04 Sep 2022
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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
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