Energy Metabolism in Neurodegenerative Diseases

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (25 April 2024) | Viewed by 1270

Special Issue Editors


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Guest Editor
Department of Biochemistry, Faculty of Medicine, Medical University of Gdansk, Gdansk, Poland
Interests: energy metabolism; animal models; huntington’s disease; neurodegener-ative diseases; heart; skeletal muscle
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Guest Editor
Department of Molecular Biology, Faculty of Biology, University of Gdansk, Gdansk, Poland
Interests: pathophysiology of neurodegenerative diseases; neuroinflammatory pathways; animal behavior; genetic disorders; molecular mechanisms
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The incidence of age-related disorders, specifically neurodegenerative diseases, has been on the rise in correlation with the increase in life expectancy observed over the past century. Diseases such as Alzheimer's, Parkinson's, Huntington's, and multiple sclerosis are chronic conditions characterized by the progressive loss of neurons in various motor, sensory, or cognitive systems. A growing body of evidence suggests a strong link between metabolic dysregulation and the pathogenesis of neurodegeneration. Metabolic changes, such as alterations in energy metabolism, oxidative stress, and mitochondrial dysfunction, have emerged as key contributors to the neurodegenerative process. These metabolic disturbances can disrupt cellular homeostasis, impair neuronal function, and ultimately lead to neuronal death. Understanding the intricate interplay between metabolic alterations and neurodegeneration is of the utmost importance in unraveling the underlying mechanisms of these age-related disorders and identifying potential therapeutic targets.

This Special Issue will highlight new insights into energy metabolism in neurodegenerative diseases. Moreover, studies that focus on the identification of biomarkers, therapeutic targets, and future treatments related to metabolic pathways are also welcome.

Dr. Marta Tomczyk
Dr. Magdalena Podlacha
Guest Editors

Manuscript Submission Information

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Keywords

  • energy metabolism
  • neurodegeneration
  • neurodegenerative disease
  • Alzheimer’s disease
  • Parkinson’s disease
  • Huntington’s disease
  • amyotrophic lateral sclerosis
  • spinal muscular atrophy
  • Lewy body disease
  • multiple sclerosis

Published Papers (1 paper)

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Research

16 pages, 2886 KiB  
Article
In Vitro Astroglial Dysfunction Induced by Neurotoxins: Mimicking Astrocytic Metabolic Alterations of Alzheimer’s Disease
by Jéssica Taday, Fernanda Telles Fróes, Marina Seady, Carlos Alberto Gonçalves and Marina Concli Leite
Metabolites 2024, 14(3), 151; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo14030151 - 01 Mar 2024
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Abstract
Astrocytes play fundamental roles in the maintenance of brain homeostasis. The dysfunction of these cells is widely associated with brain disorders, which are often characterized by variations in the astrocyte protein markers GFAP and S100B, in addition to alterations in some of its [...] Read more.
Astrocytes play fundamental roles in the maintenance of brain homeostasis. The dysfunction of these cells is widely associated with brain disorders, which are often characterized by variations in the astrocyte protein markers GFAP and S100B, in addition to alterations in some of its metabolic functions. To understand the role of astrocytes in neurodegeneration mechanisms, we induced some of these metabolic alterations, such as energy metabolism, using methylglyoxal (MG) or fluorocitrate (FC); and neuroinflammation, using lipopolysaccharide (LPS) and streptozotocin (STZ), which is used for inducing Alzheimer’s disease (AD) in animal models. We showed that MG, LPS, STZ and FC similarly caused astrocyte dysfunction by increasing GFAP and reducing S100B secretion. In the context of AD, STZ caused an amyloid metabolism impairment verified by increases in Aβ1-40 peptide content and decreases in the amyloid degradation enzymes, IDE and NEP. Our data contribute to the understanding of the role of astrocytes in brain injury mechanisms and suggest that STZ is suitable for use in vitro models for studying the role of astrocytes in AD. Full article
(This article belongs to the Special Issue Energy Metabolism in Neurodegenerative Diseases)
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