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Lipid Mediated Mechanisms in Neurologic and Neuropsychiatric Disease
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Lipid Mediated Mechanisms in Neurologic and Neuropsychiatric Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 16493

Special Issue Editor

Prof. Dr. Irmgard Tegeder

E-Mail Website
Guest Editor
Pharmazentrum Frankfurt, Dept. of Clinical Pharmacology, Goethe-University of Frankfurt, Theodor Stern Kai 7, Bd. 74, 4th Fl, 60590 Frankfurt am Main, Germany
Interests: nerve injury and neuropathic pain; pain and aging; central adaptations to chronic pain; multiple sclerosis; neuroinflammation; neuro-immunologic communication; redox signaling; nitric oxide; endocannabinoids and other lipid signaling molecules; progranulin; autophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent advances in synulein pathology have identified specific lipids and "lipid-genes" as amplifiers of alpha synuclein's toxicity. In particular, sporadic Parkinson's disease has been associated with heterozygous mutations of acidic glucocerebrosidase (GBA), a lysosomal enzyme that degrades glucosylceramides. GlcCer accumulation has also been associated with multiple system atrophy and amyotrophic lateral sclerosis. Further ceramide species contribute to the pathology of sensory polyneuropathies. Ceramides are also increased in psychiatric diseases, such as major depression, and the inhibition of ceramide synthesis was shown to reduce depression-like behavior in animal models. The molecular mechanisms of ceramide-associated neuropathology are still incompletely understood. The accumulation of neutral lipids in neurons has been shown to recognize degenerating neurons at an early stage, and efforts are made to reduce the synthesis of monounsaturated fatty acids. An example is the targeting of stearoyl CoA desaturase, which shall reduce the burden of MUFAs and thereby the accumulation of patologic proteins. It has long been recognized that the risk for Alzheimers' disease is modulated by lipoprotein E subtypes and cholesterol biology.

This Special Issue shall be a collection of papers addressing pathologic changes and functions/mechanisms of lipid genes, individual lipids or lipid profiles in patients or in vitro/in vivo disease models. Papers may also describe novel methods for lipid analysis, visualization, or pharmacologic targeting. Original research papers and reviews are equally welcome. The Special Issue shall unravel common and specific mechanisms of lipid signaling molecules, such as ceramides and other sphingolipids and fatty acid-derived lipids that contribute to neurologic or neuropsychiatric diseases, including, for example, synucleopathies and other movement disorders, epilepsy, polyneuropathies, polyglutamine diseases, major depression and bipolar disorder, autism spectrum diseases, eating disorders and schizophrenia.

Prof. Dr. Irmgard Tegeder
Guest Editor

Manuscript Submission Information

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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.

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Keywords

  • ceramides
  • glucosylceramides
  • sphingolipids
  • gangliosides
  • fatty acids and FA-derived lipids such as prostaglandins, endocannabinoids Lysophospholipids
  • triglycerides, cholesterol
  • synucleopathies such as PD, multiple system atrophy, lewi body disease Neurodegenerative disease such as Alzheimer's disease, frontotemporal dementia Polyglutamine diseases
  • peripheral (poly)neuropathy
  • posttraumatic encephalopathy
  • major depression / bipolar disorder
  • schizophrenia
  • autism spectrum diseases
  • attention deficit disorder
  • posttraumatic stress disorder

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Published Papers (4 papers)

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Research

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18 pages, 10825 KiB  
Article
AmyP53 Prevents the Formation of Neurotoxic β-Amyloid Oligomers through an Unprecedent Mechanism of Interaction with Gangliosides: Insights for Alzheimer’s Disease Therapy
by Fodil Azzaz, Henri Chahinian, Nouara Yahi, Jacques Fantini and Coralie Di Scala
Int. J. Mol. Sci. 2023, 24(2), 1760; https://doi.org/10.3390/ijms24021760 - 16 Jan 2023
Cited by 10 | Viewed by 3201
Abstract
A broad range of data identify Ca2+-permeable amyloid pores as the most neurotoxic species of Alzheimer’s β-amyloid peptide (Aβ1–42). Following the failures of clinical trials targeting amyloid plaques by immunotherapy, a consensus is gradually emerging to change the paradigm, [...] Read more.
A broad range of data identify Ca2+-permeable amyloid pores as the most neurotoxic species of Alzheimer’s β-amyloid peptide (Aβ1–42). Following the failures of clinical trials targeting amyloid plaques by immunotherapy, a consensus is gradually emerging to change the paradigm, the strategy, and the target to cure Alzheimer’s disease. In this context, the therapeutic peptide AmyP53 was designed to prevent amyloid pore formation driven by lipid raft microdomains of the plasma membrane. Here, we show that AmyP53 outcompetes Aβ1–42 binding to lipid rafts through a unique mode of interaction with gangliosides. Using a combination of cellular, physicochemical, and in silico approaches, we unraveled the mechanism of action of AmyP53 at the atomic, molecular, and cellular levels. Molecular dynamics simulations (MDS) indicated that AmyP53 rapidly adapts its conformation to gangliosides for an optimal interaction at the periphery of a lipid raft, where amyloid pore formation occurs. Hence, we define it as an adaptive peptide. Our results describe for the first time the kinetics of AmyP53 interaction with lipid raft gangliosides at the atomic level. Physicochemical studies and in silico simulations indicated that Aβ1–42 cannot interact with lipid rafts in presence of AmyP53. These data demonstrated that AmyP53 prevents amyloid pore formation and cellular Ca2+ entry by competitive inhibition of Aβ1–42 binding to lipid raft gangliosides. The molecular details of AmyP53 action revealed an unprecedent mechanism of interaction with lipid rafts, offering innovative therapeutic opportunities for lipid raft and ganglioside-associated diseases, including Alzheimer’s, Parkinson’s, and related proteinopathies. Full article
(This article belongs to the Special Issue Lipid Mediated Mechanisms in Neurologic and Neuropsychiatric Disease)
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13 pages, 1217 KiB  
Article
Acid Sphingomyelinase Is a Modulator of Contextual Fear
by Iulia Zoicas and Johannes Kornhuber
Int. J. Mol. Sci. 2022, 23(6), 3398; https://doi.org/10.3390/ijms23063398 - 21 Mar 2022
Cited by 3 | Viewed by 2293
Abstract
Acid sphingomyelinase (ASM) regulates a variety of physiological processes and plays an important role in emotional behavior. The role of ASM in fear-related behavior has not been investigated so far. Using transgenic mice overexpressing ASM (ASMtg) and ASM deficient mice, we studied whether [...] Read more.
Acid sphingomyelinase (ASM) regulates a variety of physiological processes and plays an important role in emotional behavior. The role of ASM in fear-related behavior has not been investigated so far. Using transgenic mice overexpressing ASM (ASMtg) and ASM deficient mice, we studied whether ASM regulates fear learning and expression of cued and contextual fear in a classical fear conditioning paradigm, a model used to investigate specific attributes of post-traumatic stress disorder (PTSD). We show that ASM does not affect fear learning as both ASMtg and ASM deficient mice display unaltered fear conditioning when compared to wild-type littermates. However, ASM regulates the expression of contextual fear in a sex-specific manner. While ASM overexpression enhances the expression of contextual fear in both male and female mice, ASM deficiency reduces the expression of contextual fear specifically in male mice. The expression of cued fear, however, is not regulated by ASM as ASMtg and ASM deficient mice display similar tone-elicited freezing levels. This study shows that ASM modulates the expression of contextual fear but not of cued fear in a sex-specific manner and adds a novel piece of information regarding the involvement of ASM in hippocampal-dependent aversive memory. Full article
(This article belongs to the Special Issue Lipid Mediated Mechanisms in Neurologic and Neuropsychiatric Disease)
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Review

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11 pages, 1650 KiB  
Review
Neuropathological Features of Gaucher Disease and Gaucher Disease with Parkinsonism
by Makaila L. Furderer, Ellen Hertz, Grisel J. Lopez and Ellen Sidransky
Int. J. Mol. Sci. 2022, 23(10), 5842; https://doi.org/10.3390/ijms23105842 - 23 May 2022
Cited by 10 | Viewed by 3801
Abstract
Deficient acid β-glucocerebrosidase activity due to biallelic mutations in GBA1 results in Gaucher disease (GD). Patients with this lysosomal storage disorder exhibit a wide range of associated manifestations, spanning from virtually asymptomatic adults to infants with severe neurodegeneration. While type 1 GD (GD1) [...] Read more.
Deficient acid β-glucocerebrosidase activity due to biallelic mutations in GBA1 results in Gaucher disease (GD). Patients with this lysosomal storage disorder exhibit a wide range of associated manifestations, spanning from virtually asymptomatic adults to infants with severe neurodegeneration. While type 1 GD (GD1) is considered non-neuronopathic, a small subset of patients develop parkinsonian features. Variants in GBA1 are also an important risk factor for several common Lewy body disorders (LBDs). Neuropathological examinations of patients with GD, including those who developed LBDs, are rare. GD primarily affects macrophages, and perivascular infiltration of Gaucher macrophages is the most common neuropathologic finding. However, the frequency of these clusters and the affected anatomical region varies. GD affects astrocytes, and, in neuronopathic GD, neurons in cerebral cortical layers 3 and 5, layer 4b of the calcarine cortex, and hippocampal regions CA2–4. In addition, several reports describe selective degeneration of the cerebellar dentate nucleus in chronic neuronopathic GD. GD1 is characterized by astrogliosis without prominent neuronal loss. In GD-LBD, widespread Lewy body pathology is seen, often involving hippocampal regions CA2–4. Additional neuropathological examinations in GD are sorely needed to clarify disease-specific patterns and elucidate causative mechanisms relevant to GD, and potentially to more common neurodegenerative diseases. Full article
(This article belongs to the Special Issue Lipid Mediated Mechanisms in Neurologic and Neuropsychiatric Disease)
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66 pages, 3925 KiB  
Review
Molecular Alterations of the Endocannabinoid System in Psychiatric Disorders
by Daniela Navarro, Ani Gasparyan, Francisco Navarrete, Abraham B. Torregrosa, Gabriel Rubio, Marta Marín-Mayor, Gabriela B. Acosta, Maria Salud Garcia-Gutiérrez and Jorge Manzanares
Int. J. Mol. Sci. 2022, 23(9), 4764; https://doi.org/10.3390/ijms23094764 - 26 Apr 2022
Cited by 17 | Viewed by 6130
Abstract
The therapeutic benefits of the current medications for patients with psychiatric disorders contrast with a great variety of adverse effects. The endocannabinoid system (ECS) components have gained high interest as potential new targets for treating psychiatry diseases because of their neuromodulator role, which [...] Read more.
The therapeutic benefits of the current medications for patients with psychiatric disorders contrast with a great variety of adverse effects. The endocannabinoid system (ECS) components have gained high interest as potential new targets for treating psychiatry diseases because of their neuromodulator role, which is essential to understanding the regulation of many brain functions. This article reviewed the molecular alterations in ECS occurring in different psychiatric conditions. The methods used to identify alterations in the ECS were also described. We used a translational approach. The animal models reproducing some behavioral and/or neurochemical aspects of psychiatric disorders and the molecular alterations in clinical studies in post-mortem brain tissue or peripheral tissues were analyzed. This article reviewed the most relevant ECS changes in prevalent psychiatric diseases such as mood disorders, schizophrenia, autism, attentional deficit, eating disorders (ED), and addiction. The review concludes that clinical research studies are urgently needed for two different purposes: (1) To identify alterations of the ECS components potentially useful as new biomarkers relating to a specific disease or condition, and (2) to design new therapeutic targets based on the specific alterations found to improve the pharmacological treatment in psychiatry. Full article
(This article belongs to the Special Issue Lipid Mediated Mechanisms in Neurologic and Neuropsychiatric Disease)
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