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Metabolomics in Neurodegenerative Disease
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Metabolomics in Neurodegenerative Disease

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 (31 December 2018) | Viewed by 50948

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editor

Dr. Brian Green

E-Mail Website
Guest Editor
School of Biological Sciences, Queen's University Belfast, University Road, Belfast BT7 1NN, Northern Ireland, UK
Interests: metabolomics; neurodegenerative disease; diet; nutrition; Alzheimer’s diesease

Special Issue Information

Dear Colleagues,

The range of human neurodegenerative diseases continues to pose significant unmet medical needs for societies around the world. Examples of common neurodegenerative diseases include multiple sclerosis, amyotrophic lateral sclerosis, age-related macular degeneration, vascular dementia, Alzheimer's, Parkinson's, and Huntington's disease. The progressive and terminal nature of these conditions places a considerable personal burden on the individual affected. Additionally, there is a growing economic and public health burden which forces governments and health services to make difficult choices concerning the allocation of medical resources. Tens of millions of people are indiscriminately affected by various dementias which are rising at an alarming rate. There are no cures for many conditions and it is clear that treatments applied as early as possible could greatly improve outcomes for patients. Therefore, new disease classification and diagnostic tools should be a key priority. Metabolomics represents a relatively new field of analytical science which can be extremely useful in the early diagnosis of disease. The relatively unique feature of metabolites is that they sit at the intersection between the genetic background of an organism and its environment. Since many neurodegenerative diseases are not genetically inherited (instead having range of known genetic risk factors and also a large number of unknown environmental triggers) metabolomics offers great promise for the discovery of new, biologically, and clinically relevant biomarkers for neurodegenerative disorders. It is already bringing forward new knowledge in terms of the mechanisms of neurodegenerative disease.

The present Special Issue of Metabolites presents a collection of cutting-edge studies and review articles demonstrating the application of metabolomics for the investigation of neurodegenerative disease.

Dr. Brian D. Green
Guest Editor

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

  • metabolomics Parkinson's disease
  • metabolomics Huntington's disease
  • metabolomics Alzheimer's disease
  • disease multiple sclerosis
  • metabolomics amyotrophic lateral sclerosis
  • metabolomics vascular dementia

Published Papers (11 papers)

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Editorial

Jump to: Research, Review

2 pages, 138 KiB  
Editorial
The Application of Metabolomic Techniques in Research Investigating Neurodegenerative Diseases
by Brian D. Green
Metabolites 2019, 9(12), 283; https://doi.org/10.3390/metabo9120283 - 20 Nov 2019
Viewed by 1904
Abstract
We live in a world posing many new and different challenges for human health, and one such challenge is the rapidly expanding number of cases of human neurodegenerative disease [...] Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)

Research

Jump to: Editorial, Review

13 pages, 2046 KiB  
Article
In Vivo Microdialysis of Endogenous and 13C-labeled TCA Metabolites in Rat Brain: Reversible and Persistent Effects of Mitochondrial Inhibition and Transient Cerebral Ischemia
by Jesper F. Havelund, Kevin H. Nygaard, Troels H. Nielsen, Carl-Henrik Nordström, Frantz R. Poulsen, Nils. J. Færgeman, Axel Forsse and Jan Bert Gramsbergen
Metabolites 2019, 9(10), 204; https://doi.org/10.3390/metabo9100204 - 27 Sep 2019
Cited by 3 | Viewed by 4067
Abstract
Cerebral micro-dialysis allows continuous sampling of extracellular metabolites, including glucose, lactate and pyruvate. Transient ischemic events cause a rapid drop in glucose and a rise in lactate levels. Following such events, the lactate/pyruvate (L/P) ratio may remain elevated for a prolonged period of [...] Read more.
Cerebral micro-dialysis allows continuous sampling of extracellular metabolites, including glucose, lactate and pyruvate. Transient ischemic events cause a rapid drop in glucose and a rise in lactate levels. Following such events, the lactate/pyruvate (L/P) ratio may remain elevated for a prolonged period of time. In neurointensive care clinics, this ratio is considered a metabolic marker of ischemia and/or mitochondrial dysfunction. Here we propose a novel, sensitive microdialysis liquid chromatography-mass spectrometry (LC-MS) approach to monitor mitochondrial dysfunction in living brain using perfusion with 13C-labeled succinate and analysis of 13C-labeled tricarboxylic acid cycle (TCA) intermediates. This approach was evaluated in rat brain using malonate-perfusion (10–50 mM) and endothelin-1 (ET-1)-induced transient cerebral ischemia. In the malonate model, the expected changes upon inhibition of succinate dehydrogenase (SDH) were observed, i.e., an increase in endogenous succinate and decreases in fumaric acid and malic acid. The inhibition was further elaborated by incorporation of 13C into specific TCA intermediates from 13C-labeled succinate. In the ET-1 model, increases in non-labeled TCA metabolites (reflecting release of intracellular compounds) and decreases in 13C-labeled TCA metabolites (reflecting inhibition of de novo synthesis) were observed. The analysis of 13C incorporation provides further layers of information to identify metabolic disturbances in experimental models and neuro-intensive care patients. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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14 pages, 2143 KiB  
Article
Palmitate and Stearate are Increased in the Plasma in a 6-OHDA Model of Parkinson’s Disease
by Anuri Shah, Pei Han, Mung-Yee Wong, Raymond Chuen-Chung Chang and Cristina Legido-Quigley
Metabolites 2019, 9(2), 31; https://doi.org/10.3390/metabo9020031 - 13 Feb 2019
Cited by 15 | Viewed by 4639
Abstract
Introduction: Parkinson’s disease (PD) is the second most common neurodegenerative disorder, without any widely available curative therapy. Metabolomics is a powerful tool which can be used to identify unexpected pathway-related disease progression and pathophysiological mechanisms. In this study, metabolomics in brain, plasma and [...] Read more.
Introduction: Parkinson’s disease (PD) is the second most common neurodegenerative disorder, without any widely available curative therapy. Metabolomics is a powerful tool which can be used to identify unexpected pathway-related disease progression and pathophysiological mechanisms. In this study, metabolomics in brain, plasma and liver was investigated in an experimental PD model, to discover small molecules that are associated with dopaminergic cell loss. Methods: Sprague Dawley (SD) rats were injected unilaterally with 6-hydroxydopamine (6-OHDA) or saline for the vehicle control group into the medial forebrain bundle (MFB) to induce loss of dopaminergic neurons in the substantia nigra pars compacta. Plasma, midbrain and liver samples were collected for metabolic profiling. Multivariate and univariate analyses revealed metabolites that were altered in the PD group. Results: In plasma, palmitic acid (q = 3.72 × 10−2, FC = 1.81) and stearic acid (q = 3.84 × 10−2, FC = 2.15), were found to be increased in the PD group. Palmitic acid (q = 3.5 × 10−2) and stearic acid (q = 2.7 × 10−2) correlated with test scores indicative of motor dysfunction. Monopalmitin (q = 4.8 × 10−2, FC = −11.7), monostearin (q = 3.72 × 10−2, FC = −15.1) and myo-inositol (q = 3.81 × 10−2, FC = −3.32), were reduced in the midbrain. The liver did not have altered levels of these molecules. Conclusion: Our results show that saturated free fatty acids, their monoglycerides and myo-inositol metabolism in the midbrain and enteric circulation are associated with 6-OHDA-induced PD pathology. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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16 pages, 716 KiB  
Article
Metabolomic Profiling of Cerebral Palsy Brain Tissue Reveals Novel Central Biomarkers and Biochemical Pathways Associated with the Disease: A Pilot Study
by Zeynep Alpay Savasan, Ali Yilmaz, Zafer Ugur, Buket Aydas, Ray O. Bahado-Singh and Stewart F. Graham
Metabolites 2019, 9(2), 27; https://doi.org/10.3390/metabo9020027 - 02 Feb 2019
Cited by 17 | Viewed by 4254
Abstract
Cerebral palsy (CP) is one of the most common causes of motor disability in childhood, with complex and heterogeneous etiopathophysiology and clinical presentation. Understanding the metabolic processes associated with the disease may aid in the discovery of preventive measures and therapy. Tissue samples [...] Read more.
Cerebral palsy (CP) is one of the most common causes of motor disability in childhood, with complex and heterogeneous etiopathophysiology and clinical presentation. Understanding the metabolic processes associated with the disease may aid in the discovery of preventive measures and therapy. Tissue samples (caudate nucleus) were obtained from post-mortem CP cases (n = 9) and age- and gender-matched control subjects (n = 11). We employed a targeted metabolomics approach using both 1H NMR and direct injection liquid chromatography-tandem mass spectrometry (DI/LC-MS/MS). We accurately identified and quantified 55 metabolites using 1H NMR and 186 using DI/LC-MS/MS. Among the 222 detected metabolites, 27 showed significant concentration changes between CP cases and controls. Glycerophospholipids and urea were the most commonly selected metabolites used to develop predictive models capable of discriminating between CP and controls. Metabolomics enrichment analysis identified folate, propanoate, and androgen/estrogen metabolism as the top three significantly perturbed pathways. We report for the first time the metabolomic profiling of post-mortem brain tissue from patients who died from cerebral palsy. These findings could help to further investigate the complex etiopathophysiology of CP while identifying predictive, central biomarkers of CP. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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10 pages, 1259 KiB  
Article
Metabolomic Profiling of Bile Acids in an Experimental Model of Prodromal Parkinson’s Disease
by Stewart F. Graham, Nolwen L. Rey, Zafer Ugur, Ali Yilmaz, Eric Sherman, Michael Maddens, Ray O. Bahado-Singh, Katelyn Becker, Emily Schulz, Lindsay K. Meyerdirk, Jennifer A. Steiner, Jiyan Ma and Patrik Brundin
Metabolites 2018, 8(4), 71; https://doi.org/10.3390/metabo8040071 - 31 Oct 2018
Cited by 34 | Viewed by 4866
Abstract
For people with Parkinson’s disease (PD), considered the most common neurodegenerative disease behind Alzheimer’s disease, accurate diagnosis is dependent on many factors; however, misdiagnosis is extremely common in the prodromal phases of the disease, when treatment is thought to be most effective. Currently, [...] Read more.
For people with Parkinson’s disease (PD), considered the most common neurodegenerative disease behind Alzheimer’s disease, accurate diagnosis is dependent on many factors; however, misdiagnosis is extremely common in the prodromal phases of the disease, when treatment is thought to be most effective. Currently, there are no robust biomarkers that aid in the early diagnosis of PD. Following previously reported work by our group, we accurately measured the concentrations of 18 bile acids in the serum of a prodromal mouse model of PD. We identified three bile acids at significantly different concentrations (p < 0.05) when mice representing a prodromal PD model were compared with controls. These include ω-murichoclic acid (MCAo), tauroursodeoxycholic acid (TUDCA) and ursodeoxycholic acid (UDCA). All were down-regulated in prodromal PD mice with TUDCA and UDCA at significantly lower levels (17-fold and 14-fold decrease, respectively). Using the concentration of three bile acids combined with logistic regression, we can discriminate between prodromal PD mice from control mice with high accuracy (AUC (95% CI) = 0.906 (0.777–1.000)) following cross validation. Our study highlights the need to investigate bile acids as potential biomarkers that predict PD and possibly reflect the progression of manifest PD. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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16 pages, 787 KiB  
Article
Evidence That Parietal Lobe Fatty Acids May Be More Profoundly Affected in Moderate Alzheimer’s Disease (AD) Pathology Than in Severe AD Pathology
by Muhammad L. Nasaruddin, Xiaobei Pan, Bernadette McGuinness, Peter Passmore, Patrick G. Kehoe, Christian Hölscher, Stewart F. Graham and Brian D. Green
Metabolites 2018, 8(4), 69; https://doi.org/10.3390/metabo8040069 - 26 Oct 2018
Cited by 16 | Viewed by 3910
Abstract
Brain is a lipid-rich tissue, and fatty acids (FAs) play a crucial role in brain function, including neuronal cell growth and development. This study used GC-MS to survey all detectable FAs in the human parietal cortex (Brodmann area 7). These FAs were accurately [...] Read more.
Brain is a lipid-rich tissue, and fatty acids (FAs) play a crucial role in brain function, including neuronal cell growth and development. This study used GC-MS to survey all detectable FAs in the human parietal cortex (Brodmann area 7). These FAs were accurately quantified in 27 cognitively normal age-matched controls, 16 cases of moderate Alzheimer’s disease (AD), 30 severe AD, and 14 dementia with Lewy bodies (DLB). A total of 24 FA species were identified. Multiple comparison procedures, using stepdown permutation tests, noted higher levels of 13 FAs but the majority of changes were in moderate AD and DLB, rather than severe AD. Subjects with moderate AD and DLB pathology exhibited significantly higher levels of a number of FAs (13 FAs and 12 FAs, respectively). These included nervonic, lignoceric, cis-13,16-docosadienoic, arachidonic, cis-11,14,17-eicosatrienoic, erucic, behenic, α-linolenic, stearic, oleic, cis-10-heptanoic, and palmitic acids. The similarities between moderate AD and DLB were quite striking—arachidic acid was the only FA which was higher in moderate AD than control, and was not similarly affected in DLB. Furthermore, there were no significant differences between moderate AD and DLB. The associations between each FA and a number of variables, including diagnosis, age, gender, Aβ plaque load, tau load, and frontal tissue pH, were also investigated. To conclude, the development of AD or DLB pathology affects brain FA composition but, intriguingly, moderate AD neuropathology impacts this to a much greater extent. Post-mortem delay is a potential confounding factor, but the findings here suggest that there could be a more dynamic metabolic response in the earlier stages of the disease pathology. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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20 pages, 1630 KiB  
Article
Potential Metabolomic Linkage in Blood between Parkinson’s Disease and Traumatic Brain Injury
by Massimo S. Fiandaca, Thomas J. Gross, Thomas M. Johnson, Michele T. Hu, Samuel Evetts, Richard Wade-Martins, Kian Merchant-Borna, Jeffrey Bazarian, Amrita K. Cheema, Mark Mapstone and Howard J. Federoff
Metabolites 2018, 8(3), 50; https://doi.org/10.3390/metabo8030050 - 07 Sep 2018
Cited by 15 | Viewed by 5342
Abstract
The etiologic basis for sporadic forms of neurodegenerative diseases has been elusive but likely represents the product of genetic predisposition and various environmental factors. Specific gene-environment interactions have become more salient owing, in part, to the elucidation of epigenetic mechanisms and their impact [...] Read more.
The etiologic basis for sporadic forms of neurodegenerative diseases has been elusive but likely represents the product of genetic predisposition and various environmental factors. Specific gene-environment interactions have become more salient owing, in part, to the elucidation of epigenetic mechanisms and their impact on health and disease. The linkage between traumatic brain injury (TBI) and Parkinson’s disease (PD) is one such association that currently lacks a mechanistic basis. Herein, we present preliminary blood-based metabolomic evidence in support of potential association between TBI and PD. Using untargeted and targeted high-performance liquid chromatography-mass spectrometry we identified metabolomic biomarker profiles in a cohort of symptomatic mild TBI (mTBI) subjects (n = 75) 3–12 months following injury (subacute) and TBI controls (n = 20), and a PD cohort with known PD (n = 20) or PD dementia (PDD) (n = 20) and PD controls (n = 20). Surprisingly, blood glutamic acid levels in both the subacute mTBI (increased) and PD/PDD (decreased) groups were notably altered from control levels. The observed changes in blood glutamic acid levels in mTBI and PD/PDD are discussed in relation to other metabolite profiling studies. Should our preliminary results be replicated in comparable metabolomic investigations of TBI and PD cohorts, they may contribute to an “excitotoxic” linkage between TBI and PD/PDD. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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Review

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18 pages, 1292 KiB  
Review
Imaging Mass Spectrometry: A New Tool to Assess Molecular Underpinnings of Neurodegeneration
by Kevin Chen, Dodge Baluya, Mehmet Tosun, Feng Li and Mirjana Maletic-Savatic
Metabolites 2019, 9(7), 135; https://doi.org/10.3390/metabo9070135 - 10 Jul 2019
Cited by 30 | Viewed by 4259
Abstract
Neurodegenerative diseases are prevalent and devastating. While extensive research has been done over the past decades, we are still far from comprehensively understanding what causes neurodegeneration and how we can prevent it or reverse it. Recently, systems biology approaches have led to a [...] Read more.
Neurodegenerative diseases are prevalent and devastating. While extensive research has been done over the past decades, we are still far from comprehensively understanding what causes neurodegeneration and how we can prevent it or reverse it. Recently, systems biology approaches have led to a holistic examination of the interactions between genome, metabolome, and the environment, in order to shed new light on neurodegenerative pathogenesis. One of the new technologies that has emerged to facilitate such studies is imaging mass spectrometry (IMS). With its ability to map a wide range of small molecules with high spatial resolution, coupled with the ability to quantify them at once, without the need for a priori labeling, IMS has taken center stage in current research efforts in elucidating the role of the metabolome in driving neurodegeneration. IMS has already proven to be effective in investigating the lipidome and the proteome of various neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, Huntington’s, multiple sclerosis, and amyotrophic lateral sclerosis. Here, we review the IMS platform for capturing biological snapshots of the metabolic state to shed more light on the molecular mechanisms of the diseased brain. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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36 pages, 2023 KiB  
Review
Metabolomics and Age-Related Macular Degeneration
by Connor N. Brown, Brian D. Green, Richard B. Thompson, Anneke I. Den Hollander, Imre Lengyel and On behalf of the EYE-RISK consortium
Metabolites 2019, 9(1), 4; https://doi.org/10.3390/metabo9010004 - 27 Dec 2018
Cited by 38 | Viewed by 8466
Abstract
Age-related macular degeneration (AMD) leads to irreversible visual loss, therefore, early intervention is desirable, but due to its multifactorial nature, diagnosis of early disease might be challenging. Identification of early markers for disease development and progression is key for disease diagnosis. Suitable biomarkers [...] Read more.
Age-related macular degeneration (AMD) leads to irreversible visual loss, therefore, early intervention is desirable, but due to its multifactorial nature, diagnosis of early disease might be challenging. Identification of early markers for disease development and progression is key for disease diagnosis. Suitable biomarkers can potentially provide opportunities for clinical intervention at a stage of the disease when irreversible changes are yet to take place. One of the most metabolically active tissues in the human body is the retina, making the use of hypothesis-free techniques, like metabolomics, to measure molecular changes in AMD appealing. Indeed, there is increasing evidence that metabolic dysfunction has an important role in the development and progression of AMD. Therefore, metabolomics appears to be an appropriate platform to investigate disease-associated biomarkers. In this review, we explored what is known about metabolic changes in the retina, in conjunction with the emerging literature in AMD metabolomics research. Methods for metabolic biomarker identification in the eye have also been discussed, including the use of tears, vitreous, and aqueous humor, as well as imaging methods, like fluorescence lifetime imaging, that could be translated into a clinical diagnostic tool with molecular level resolution. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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19 pages, 4052 KiB  
Review
No Country for Old Worms: A Systematic Review of the Application of C. elegans to Investigate a Bacterial Source of Environmental Neurotoxicity in Parkinson’s Disease
by Kim A. Caldwell, Jennifer L. Thies and Guy A. Caldwell
Metabolites 2018, 8(4), 70; https://doi.org/10.3390/metabo8040070 - 29 Oct 2018
Cited by 8 | Viewed by 4233
Abstract
While progress has been made in discerning genetic associations with Parkinson’s disease (PD), identifying elusive environmental contributors necessitates the application of unconventional hypotheses and experimental strategies. Here, we provide an overview of studies that we conducted on a neurotoxic metabolite produced by a [...] Read more.
While progress has been made in discerning genetic associations with Parkinson’s disease (PD), identifying elusive environmental contributors necessitates the application of unconventional hypotheses and experimental strategies. Here, we provide an overview of studies that we conducted on a neurotoxic metabolite produced by a species of common soil bacteria, Streptomyces venezuelae (S. ven), indicating that the toxicity displayed by this bacterium causes stress in diverse cellular mechanisms, such as the ubiquitin proteasome system and mitochondrial homeostasis. This dysfunction eventually leads to age and dose-dependent neurodegeneration in the nematode Caenorhabditis elegans. Notably, dopaminergic neurons have heightened susceptibility, but all of the neuronal classes eventually degenerate following exposure. Toxicity further extends to human SH-SY5Y cells, which also degenerate following exposure. Additionally, the neurons of nematodes expressing heterologous aggregation-prone proteins display enhanced metabolite vulnerability. These mechanistic analyses collectively reveal a unique metabolomic fingerprint for this bacterially-derived neurotoxin. In considering that epidemiological distinctions in locales influence the incidence of PD, we surveyed soils from diverse regions of Alabama, and found that exposure to ~30% of isolated Streptomyces species caused worm dopaminergic neurons to die. In addition to aging, one of the few established contributors to PD appears to be a rural lifestyle, where exposure to soil on a regular basis might increase the risk of interaction with bacteria producing such toxins. Taken together, these data suggest that a novel toxicant within the Streptomyces genus might represent an environmental contributor to the progressive neurodegeneration that is associated with PD. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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9 pages, 1954 KiB  
Review
High-Throughput Direct Mass Spectrometry-Based Metabolomics to Characterize Metabolite Fingerprints Associated with Alzheimer’s Disease Pathogenesis
by Raúl González-Domínguez, Ana Sayago and Ángeles Fernández-Recamales
Metabolites 2018, 8(3), 52; https://doi.org/10.3390/metabo8030052 - 18 Sep 2018
Cited by 20 | Viewed by 4033
Abstract
Direct mass spectrometry-based metabolomics has been widely employed in recent years to characterize the metabolic alterations underlying Alzheimer’s disease development and progression. This high-throughput approach presents great potential for fast and simultaneous fingerprinting of a vast number of metabolites, which can be applied [...] Read more.
Direct mass spectrometry-based metabolomics has been widely employed in recent years to characterize the metabolic alterations underlying Alzheimer’s disease development and progression. This high-throughput approach presents great potential for fast and simultaneous fingerprinting of a vast number of metabolites, which can be applied to multiple biological matrices including serum/plasma, urine, cerebrospinal fluid and tissues. In this review article, we present the main advantages and drawbacks of metabolomics based on direct mass spectrometry compared with conventional analytical techniques, and provide a comprehensive revision of the literature on the use of these tools in the investigation of Alzheimer’s disease. Full article
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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