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Metabolites
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Metabolomics in Neurodegenerative Diseases
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Metabolomics in Neurodegenerative Diseases

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: 5 December 2024 | Viewed by 5285

Special Issue Editors

Dr. Stewart Francis Graham

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Guest Editor
Metabolomics Department, Beaumont Research Institute, Corewell Health East William-Beaumont University Hospital, Royal Oak, MI, USA
Interests: Alzheimer’s disease; mild cognitive impairment; Parkinson’s disease; delirium; neurodegeneration; metabolomics; biomarkers; biochemistry; etiology; pathophysiology
Special Issues, Collections and Topics in MDPI journals
Dr. Nazia M. Saiyed

E-Mail Website
Guest Editor
Metabolomics Department, Beaumont Research Institute, Corewell Health East William-Beaumont University Hospital, Royal Oak, MI, USA
Interests: delirium; Alzheimer’s disease; Parkinson’s disease; metabolomics; biomarkers; biochemistry; etiology; pathophysiology
Dr. Ali Yilmaz

E-Mail Website
Guest Editor
Metabolomics Department, Beaumont Research Institute, Corewell Health East William-Beaumont University Hospital, Royal Oak, MI, USA
Interests: Alzheimer’s disease; Parkinson’s disease; TBI; multiple sclerosis; Huntington's disease; metabolomics; biomarkers; multi-omics; etiology; statistical modelling

Special Issue Information

Dear Colleagues,

Metabolomics in neurodegenerative diseases holds promise as a dynamic field elucidating molecular insights into conditions like Alzheimer's, Parkinson's, and many more. This promising discipline scrutinizes the intricate metabolic profiles of biological systems, aiding in the identification of biomarkers, unraveling disease mechanisms, and advancing diagnostic precision. By employing advanced analytical techniques, such as mass spectrometry and nuclear magnetic resonance spectroscopy, researchers scrutinize alterations in metabolite patterns associated with neurodegeneration. These alterations encompass disrupted energy metabolism, aberrant lipid processing, and amino acid imbalances, among many others, offering invaluable clues regarding the intricate pathophysiology of these diseases. Metabolomics also paves the way for novel therapeutic targets and personalized interventions. However, challenges remain in standardization, data integration, and comprehending causative relationships. This special edition of Metabolites underscores the accelerating role of metabolomics in deepening our comprehension of neurodegenerative disorders, fostering innovative diagnostic avenues and treatment strategies.

Dr. Stewart Francis Graham
Dr. Nazia M. Saiyed
Dr. Ali Yilmaz
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. Metabolites 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 2700 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

  • neurodegenerative disease
  • Alzheimer’s disease
  • Parkinson’s disease
  • Huntington’s disease
  • ALS
  • neurodegeneration
  • biomarkers
  • metabolism
  • etiology
  • pathophysiology
  • biochemistry

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Published Papers (3 papers)

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Research

15 pages, 1930 KiB  
Article
Diagnostic Potential of Alternations of Bile Acid Profiles in the Plasma of Patients with Huntington’s Disease
by Ping-I Chiang, Kuo-Hsuan Chang, Hsiang-Yu Tang, Yih-Ru Wu, Mei-Ling Cheng and Chiung-Mei Chen
Metabolites 2024, 14(7), 394; https://doi.org/10.3390/metabo14070394 - 20 Jul 2024
Viewed by 947
Abstract
Huntington’s disease (HD) is characterized by progressive involuntary chorea movements and cognitive decline. Recent research indicates that metabolic disturbance may play a role in its pathogenesis. Bile acids, produced during cholesterol metabolism in the liver, have been linked to neurodegenerative conditions. This study [...] Read more.
Huntington’s disease (HD) is characterized by progressive involuntary chorea movements and cognitive decline. Recent research indicates that metabolic disturbance may play a role in its pathogenesis. Bile acids, produced during cholesterol metabolism in the liver, have been linked to neurodegenerative conditions. This study investigated variations in plasma bile acid profiles among individuals with HD. Plasma levels of 16 primary and secondary bile acids and their conjugates were analyzed in 20 healthy controls and 33 HD patients, including 24 with symptoms (symHD) and 9 carriers in the presymptomatic stage (preHD). HD patients exhibited significantly higher levels of glycochenodeoxycholic acid (GCDCA) and glycoursodeoxycholic acid (GUDCA) compared to healthy controls. Conversely, isolithocholic acid levels were notably lower in the HD group. Neurotoxic bile acids (glycocholic acid (GCA) + glycodeoxycholic acid (GDCA) + GCDCA) were elevated in symHD patients, while levels of neuroprotective bile acids (ursodeoxycholic acid (UDCA) + GUDCA + tauroursodeoxycholic acid (TUDCA)) were higher in preHD carriers, indicating a compensatory response to early neuronal damage. These results underscore the importance of changes in plasma bile acid profiles in HD and their potential involvement in disease mechanisms. The identified bile acids (GCDCA, GUDCA, and isolithocholic acid) could potentially serve as markers to distinguish between HD stages and healthy individuals. Nonetheless, further research is warranted to fully understand the clinical implications of these findings and their potential as diagnostic or therapeutic tools for HD. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Diseases)
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17 pages, 3018 KiB  
Article
Disturbances in Muscle Energy Metabolism in Patients with Amyotrophic Lateral Sclerosis
by Petra Parvanovova, Petra Hnilicova, Martin Kolisek, Zuzana Tatarkova, Erika Halasova, Egon Kurca, Simona Holubcikova, Monika Turcanova Koprusakova and Eva Baranovicova
Metabolites 2024, 14(7), 356; https://doi.org/10.3390/metabo14070356 - 23 Jun 2024
Viewed by 1376
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease type of motor neuron disorder characterized by degeneration of the upper and lower motor neurons resulting in dysfunction of the somatic muscles of the body. The ALS condition is manifested in progressive skeletal muscle [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease type of motor neuron disorder characterized by degeneration of the upper and lower motor neurons resulting in dysfunction of the somatic muscles of the body. The ALS condition is manifested in progressive skeletal muscle atrophy and spasticity. It leads to death, mostly due to respiratory failure. Within the pathophysiology of the disease, muscle energy metabolism seems to be an important part. In our study, we used blood plasma from 25 patients with ALS diagnosed by definitive El Escorial criteria according to ALSFR-R (Revised Amyotrophic Lateral Sclerosis Functional Rating Scale) criteria and 25 age and sex-matched subjects. Aside from standard clinical biochemical parameters, we used the NMR (nuclear magnetic resonance) metabolomics approach to determine relative plasma levels of metabolites. We observed a decrease in total protein level in blood; however, despite accelerated skeletal muscle catabolism characteristic for ALS patients, we did not detect changes in plasma levels of essential amino acids. When focused on alterations in energy metabolism within muscle, compromised creatine uptake was accompanied by decreased plasma creatinine. We did not observe changes in plasma levels of BCAAs (branched chain amino acids; leucine, isoleucine, valine); however, the observed decrease in plasma levels of all three BCKAs (branched chain alpha-keto acids derived from BCAAs) suggests enhanced utilization of BCKAs as energy substrate. Glutamine, found to be increased in blood plasma in ALS patients, besides serving for ammonia detoxification, could also be considered a potential TCA (tricarboxylic acid) cycle contributor in times of decreased pyruvate utilization. When analyzing the data by using a cross-validated Random Forest algorithm, it finished with an AUC of 0.92, oob error of 8%, and an MCC (Matthew’s correlation coefficient) of 0.84 when relative plasma levels of metabolites were used as input variables. Although the discriminatory power of the system used was promising, additional features are needed to create a robust discriminatory model. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Diseases)
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12 pages, 968 KiB  
Article
Assessing the Biological Mechanisms Linking Smoking Behavior and Cognitive Function: A Mediation Analysis of Untargeted Metabolomics
by Jerome J. Choi, Rebecca L. Koscik, Erin M. Jonaitis, Daniel J. Panyard, Autumn R. Morrow, Sterling C. Johnson, Corinne D. Engelman and Lauren L. Schmitz
Metabolites 2023, 13(11), 1154; https://doi.org/10.3390/metabo13111154 - 16 Nov 2023
Viewed by 1895
Abstract
(1) Smoking is the most significant preventable health hazard in the modern world. It increases the risk of vascular problems, which are also risk factors for dementia. In addition, toxins in cigarettes increase oxidative stress and inflammation, which have both been linked to [...] Read more.
(1) Smoking is the most significant preventable health hazard in the modern world. It increases the risk of vascular problems, which are also risk factors for dementia. In addition, toxins in cigarettes increase oxidative stress and inflammation, which have both been linked to the development of Alzheimer’s disease and related dementias (ADRD). This study identified potential mechanisms of the smoking–cognitive function relationship using metabolomics data from the longitudinal Wisconsin Registry for Alzheimer’s Prevention (WRAP). (2) 1266 WRAP participants were included to assess the association between smoking status and four cognitive composite scores. Next, untargeted metabolomic data were used to assess the relationships between smoking and metabolites. Metabolites significantly associated with smoking were then tested for association with cognitive composite scores. Total effect models and mediation models were used to explore the role of metabolites in smoking-cognitive function pathways. (3) Plasma N-acetylneuraminate was associated with smoking status Preclinical Alzheimer Cognitive Composite 3 (PACC3) and Immediate Learning (IMM). N-acetylneuraminate mediated 12% of the smoking-PACC3 relationship and 13% of the smoking-IMM relationship. (4) These findings provide links between previous studies that can enhance our understanding of potential biological pathways between smoking and cognitive function. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Diseases)
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