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Impact of Lipid Homeostasis in Neurodegenerative Diseases
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Impact of Lipid Homeostasis in Neurodegenerative Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (15 July 2023) | Viewed by 24760

Special Issue Editor

Dr. Marcus O. W. Grimm

E-Mail Website
Guest Editor
1. Nutrition Therapy and Counseling, Campus Rheinland, SRH University of Applied Health Sciences, 51377 Leverkusen, Germany
2. Experimental Neurology, Saarland University, Kirrberger Str. 1, 66421 Homburg, Saarland, Germany
3. Deutsches Institut für Demenzprävention, Saarland University, 66424 Homburg, Germany
Interests: link between lipid homeostasis and neurodegenerative diseases focusing on Alzheimer's disease; molecular biology; biochemical assays; enzymatic assays; lipid analytics; mass spectrometry; protein and cell biology; lipid protein interactions; metabolomic and nutritional approaches

Special Issue Information

Dear Colleagues,

Due to increasing life expectancy, especially in the western population, neurodegenerative diseases are becoming more and more important. Several lines of evidence suggest a close link between changes in lipid homeostasis and these neurodegenerative diseases.

The goal of this Special Issue is to gain a better understanding of the role of lipids and lipid homeostasis in the pathology of neurodegenerative diseases and to identify therapeutics that are either lipid-based or target lipid-related metabolic pathways to prevent or treat these diseases. Contributions may include but are not limited to mechanistic insights between lipids and neurodegeneration and clinical and cell culture studies addressing the relationship between lipids and neurodegeneration or describing novel techniques to address this issue.

Original research papers and reviews are equally welcome.

Dr. Marcus O. W. Grimm
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • lipids
  • neurodegeneration
  • Alzheimer’s disease (AD)
  • Parkinson’s disease (PD) and other synucleinopathies
  • amyotrophic lateral sclerosis (ALS)
  • multiple sclerosis (MS)
  • Lewy body dementia (LBD)
  • frontotemporal dementia (FTD)
  • vascular dementia (VaD)
  • Huntington’s disease (HD)
  • Creutzfeldt–Jakob disease (CJD) and other prion diseases
  • motor neuron diseases (MNDs)
  • spinocerebellar ataxias (SCA)
  • spinal muscular atrophy (SMA)
  • Zellweger syndrome
  • Niemann–Pick disease
  • Krabbe diseases (KD)
  • Gaucher disease
  • Fabry disease
  • Sandhoff disease
  • metachromatic leukodystrophy
  • other lipid storage diseases
  • ApoE and other lipoproteins
  • ceramides, sphingosine, sphingosine-1-phosphate, and other sphingolipids
  • glucosylceramides, gangliosides, and other glycosylated lipids
  • sulfatides
  • cholesterol, secosteroids, and other sterols
  • mono-, Di- and trigylcerides, and other neutral lipids
  • phosphatidylcholine, phosphatidylethanolamine, phosphoglycerol, phosphatidylinositol, phosphatidic acid, phosphatidylserine
  • plasmalogens/ether lipids
  • lyso-phospholipids
  • fatty acids and fatty-acid-derived lipids
  • acyl-/acetyl-carnitines

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Published Papers (5 papers)

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Research

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13 pages, 948 KiB  
Communication
Endothelial Function in Patients with Multiple Sclerosis: The Role of GLP-1 Agonists, Lipoprotein Subfractions, and Redox Balance
by Miroslava Hardonova, Pavel Siarnik, Monika Sivakova, Bianka Sucha, Adela Penesova, Zofia Radikova, Andrea Havranova, Richard Imrich, Miroslav Vlcek, Ingrid Zitnanova, Georgi Krastev, Maria Kiacikova, Branislav Kollar and Peter Turcani
Int. J. Mol. Sci. 2023, 24(13), 11162; https://doi.org/10.3390/ijms241311162 - 6 Jul 2023
Cited by 1 | Viewed by 1702
Abstract
Introduction: Epidemiological studies have suggested an increased vascular risk in patients with multiple sclerosis (MS). There is increasing evidence of the beneficial effects of GLP-1 agonists (GLP-1a) in preventing vascular complications and slowing the progression of neurodegeneration. Our objective was to explore the [...] Read more.
Introduction: Epidemiological studies have suggested an increased vascular risk in patients with multiple sclerosis (MS). There is increasing evidence of the beneficial effects of GLP-1 agonists (GLP-1a) in preventing vascular complications and slowing the progression of neurodegeneration. Our objective was to explore the changes in the endothelial function of MS patients after 12 months of GLP-1a therapy. We also explored the role of lipoprotein subfractions and the antioxidant capacity of plasma. Methods: MS patients were enrolled in a prospective, unicentric study. GLP-1a (dulaglutide) was administered to 13 patients. The control population consisted of 12 subjects. Endothelial function was determined by peripheral arterial tonometry and expressed as reperfusion hyperemia index (RHI). Trolox equivalent antioxidant capacity (TEAC) was used to assess the total antioxidant capacity of the plasma. The levels of lipoprotein subfractions were evaluated. Results: The GLP-1a group did not have a significant change in their RHIs after 12 months (2.1 ± 0.6 vs. 2.1 ± 0.7; p = 0.807). However, a significant increase in their TEACs was observed (4.1 ± 1.4 vs. 5.2 ± 0.5 mmol/L, p = 0.010). On the contrary, the subjects in the control group had a significant worsening of their RHIs (2.1 ± 0.5 vs. 1.8 ± 0.6; p = 0.030), without significant changes in their TEACs. Except for a significant decrease in very-low-density lipoprotein (VLDL) (30.8 ± 10.2 vs. 22.6 ± 8.3 mg/dL, p = 0.043), no other significant changes in the variables were observed in the control group. VLDL levels (beta = −0.637, p = 0.001), the use of GLP-1a therapy (beta = 0.560, p = 0.003), and small LDL (beta = 0.339, p = 0.043) were the only significant variables in the model that predicted the follow-up RHI. Conclusion: Our results suggest that the application of additional GLP-1a therapy may have atheroprotective and antioxidant effects in MS patients with high MS activity and thus may prospectively mitigate their vascular risk. However, the lipoprotein profile may also play an important role in the atherogenic risk of MS subjects. Full article
(This article belongs to the Special Issue Impact of Lipid Homeostasis in Neurodegenerative Diseases)
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13 pages, 3551 KiB  
Article
Sulfatide Deficiency, an Early Alzheimer’s Lipidomic Signature, Causes Brain Ventricular Enlargement in the Absence of Classical Neuropathological Hallmarks
by Juan Pablo Palavicini, Lin Ding, Meixia Pan, Shulan Qiu, Hu Wang, Qiang Shen, Jeffrey L. Dupree and Xianlin Han
Int. J. Mol. Sci. 2023, 24(1), 233; https://doi.org/10.3390/ijms24010233 - 23 Dec 2022
Cited by 7 | Viewed by 2815
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive memory loss and a decline in activities of daily life. Ventricular enlargement has been associated with worse performance on global cognitive tests and AD. Our previous studies demonstrated that brain sulfatides, myelin-enriched lipids, [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive memory loss and a decline in activities of daily life. Ventricular enlargement has been associated with worse performance on global cognitive tests and AD. Our previous studies demonstrated that brain sulfatides, myelin-enriched lipids, are dramatically reduced in subjects at the earliest clinically recognizable AD stages via an apolipoprotein E (APOE)-dependent and isoform-specific process. Herein, we provided pre-clinical evidence that sulfatide deficiency is causally associated with brain ventricular enlargement. Specifically, taking advantage of genetic mouse models of global and adult-onset sulfatide deficiency, we demonstrated that sulfatide losses cause ventricular enlargement without significantly affecting hippocampal or whole brain volumes using histological and magnetic resonance imaging approaches. Mild decreases in sulfatide content and mild increases in ventricular areas were also observed in human APOE4 compared to APOE2 knock-in mice. Finally, we provided Western blot and immunofluorescence evidence that aquaporin-4, the most prevalent aquaporin channel in the central nervous system (CNS) that provides fast water transportation and regulates cerebrospinal fluid in the ventricles, is significantly increased under sulfatide-deficient conditions, while other major brain aquaporins (e.g., aquaporin-1) are not altered. In short, we unraveled a novel and causal association between sulfatide deficiency and ventricular enlargement. Finally, we propose putative mechanisms by which sulfatide deficiency may induce ventricular enlargement. Full article
(This article belongs to the Special Issue Impact of Lipid Homeostasis in Neurodegenerative Diseases)
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24 pages, 4840 KiB  
Article
Quantitative NMR-Based Lipoprotein Analysis Identifies Elevated HDL-4 and Triglycerides in the Serum of Alzheimer’s Disease Patients
by Georgy Berezhnoy, Christoph Laske and Christoph Trautwein
Int. J. Mol. Sci. 2022, 23(20), 12472; https://doi.org/10.3390/ijms232012472 - 18 Oct 2022
Cited by 12 | Viewed by 3241
Abstract
Alzheimer’s disease (AD) is the most common form of dementia in the elderly and has been associated with changes in lipoprotein metabolism. We performed quantitative lipoprotein analysis in a local cohort of cognitively impaired elderly and control subjects using standardized nuclear magnetic resonance [...] Read more.
Alzheimer’s disease (AD) is the most common form of dementia in the elderly and has been associated with changes in lipoprotein metabolism. We performed quantitative lipoprotein analysis in a local cohort of cognitively impaired elderly and control subjects using standardized nuclear magnetic resonance (NMR) spectroscopy. A commercially available quantitative NMR-based assay covering 112 lipoprotein main and subtype variables was used to investigate blood serum samples from a moderate cohort size of 161 persons (71 female, 90 male), including measures of quality control. Additionally, clinical metadata and cerebrospinal fluid AD biomarkers were collected and used for analysis. High-density lipoprotein (HDL) HDL-4 subfraction levels were mostly high in female individuals with mild cognitive impairment (MCI), followed by AD. Low-density lipoprotein (LDL) LDL-2 cholesterol was slightly elevated in male AD patients. HDL-2 apolipoprotein Apo-A1, HDL-2 phospholipids, and HDL-3 triglycerides were highly abundant in AD and MCI women compared to men. When considering clinical biomarkers (Aβ, tau), very low-density lipoprotein (VLDL) VLDL-1 and intermediate-density lipoprotein (IDL) triglycerides were substantially higher in AD compared to MCI. In addition, triglyceride levels correlated positively with dementia. Different lipoprotein serum patterns were identified for AD, MCI, and control subjects. Interestingly, HDL-4 and LDL-2 cholesterol parameters revealed strong gender-specific changes in the context of AD-driven dementia. As gender-based comparisons were based on smaller sub-groups with a low n-number, several statistical findings did not meet the significance threshold for multiple comparisons testing. Still, our finding suggests that serum HDL-4 parameters and various triglycerides correlate positively with AD pathology which could be a read-out of extended lipids traveling through the blood-brain barrier, supporting amyloid plaque formation processes. Thereof, we see herein a proof of concept that this quantitative NMR-based lipoprotein assay can generate important and highly interesting data for refined AD diagnosis and patient stratification, especially when larger cohorts are available. Full article
(This article belongs to the Special Issue Impact of Lipid Homeostasis in Neurodegenerative Diseases)
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Review

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30 pages, 4409 KiB  
Review
Shared Risk Factors between Dementia and Atherosclerotic Cardiovascular Disease
by Liv Tybjærg Nordestgaard, Mette Christoffersen and Ruth Frikke-Schmidt
Int. J. Mol. Sci. 2022, 23(17), 9777; https://doi.org/10.3390/ijms23179777 - 29 Aug 2022
Cited by 37 | Viewed by 12995
Abstract
Alzheimer’s disease is the most common form of dementia, and the prodromal phases of Alzheimer’s disease can last for decades. Vascular dementia is the second most common form of dementia and is distinguished from Alzheimer’s disease by evidence of previous stroke or hemorrhage [...] Read more.
Alzheimer’s disease is the most common form of dementia, and the prodromal phases of Alzheimer’s disease can last for decades. Vascular dementia is the second most common form of dementia and is distinguished from Alzheimer’s disease by evidence of previous stroke or hemorrhage and current cerebrovascular disease. A compiled group of vascular-related dementias (vascular dementia and unspecified dementia) is often referred to as non-Alzheimer dementia. Recent evidence indicates that preventing dementia by lifestyle interventions early in life with a focus on reducing cardiovascular risk factors is a promising strategy for reducing future risk. Approximately 40% of dementia cases is estimated to be preventable by targeting modifiable, primarily cardiovascular risk factors. The aim of this review is to describe the association between risk factors for atherosclerotic cardiovascular disease and the risk of Alzheimer’s disease and non-Alzheimer dementia by providing an overview of the current evidence and to shed light on possible shared pathogenic pathways between dementia and cardiovascular disease. The included risk factors are body mass index (BMI); plasma triglyceride-, high-density lipoprotein (HDL) cholesterol-, low-density lipoprotein (LDL) cholesterol-, and total cholesterol concentrations; hypertension; diabetes; non-alcoholic fatty liver disease (NAFLD); physical inactivity; smoking; diet; the gut microbiome; and genetics. Furthermore, we aim to disentangle the difference between associations of risk factors in midlife as compared with in late life. Full article
(This article belongs to the Special Issue Impact of Lipid Homeostasis in Neurodegenerative Diseases)
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Other

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17 pages, 1793 KiB  
Brief Report
Gemfibrozil-Induced Intracellular Triglyceride Increase in SH-SY5Y, HEK and Calu-3 Cells
by Cornel Manuel Bachmann, Daniel Janitschke, Anna Andrea Lauer, Tobias Erhardt, Tobias Hartmann, Marcus Otto Walter Grimm and Heike Sabine Grimm
Int. J. Mol. Sci. 2023, 24(3), 2972; https://doi.org/10.3390/ijms24032972 - 3 Feb 2023
Cited by 2 | Viewed by 2969
Abstract
Gemfibrozil is a drug that has been used for over 40 years to lower triglycerides in blood. As a ligand for peroxisome proliferative-activated receptor-alpha (PPARα), which is expressed in many tissues, it induces the transcription of numerous genes for carbohydrate and lipid-metabolism. However, [...] Read more.
Gemfibrozil is a drug that has been used for over 40 years to lower triglycerides in blood. As a ligand for peroxisome proliferative-activated receptor-alpha (PPARα), which is expressed in many tissues, it induces the transcription of numerous genes for carbohydrate and lipid-metabolism. However, nothing is known about how intracellular lipid-homeostasis and, in particular, triglycerides are affected. As triglycerides are stored in lipid-droplets, which are known to be associated with many diseases, such as Alzheimer’s disease, cancer, fatty liver disease and type-2 diabetes, treatment with gemfibrozil could adversely affect these diseases. To address the question whether gemfibrozil also affects intracellular lipid-levels, SH-SY5Y, HEK and Calu-3 cells, representing three different metabolically active organs (brain, lung and kidney), were incubated with gemfibrozil and subsequently analyzed semi-quantitatively by mass-spectrometry. Importantly, all cells showed a strong increase in intracellular triglycerides (SH-SY5Y: 170.3%; HEK: 272.1%; Calu-3: 448.1%), suggesting that the decreased triglyceride-levels might be due to an enhanced cellular uptake. Besides the common intracellular triglyceride increase, a cell-line specific alteration in acylcarnitines are found, suggesting that especially in neuronal cell lines gemfibrozil increases the transport of fatty acids to mitochondria and therefore increases the turnover of fatty acids for the benefit of additional energy supply, which could be important in diseases, such as Alzheimer’s disease. Full article
(This article belongs to the Special Issue Impact of Lipid Homeostasis in Neurodegenerative Diseases)
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