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      Phospholipidomics in Clinical Trials for Brain Disorders: Advancing our Understanding and Therapeutic Potentials

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          Abstract

          Abstract

          Phospholipidomics is a specialized branch of lipidomics that focuses on the characterization and quantification of phospholipids. By using sensitive analytical techniques, phospholipidomics enables researchers to better understand the metabolism and activities of phospholipids in brain disorders such as Alzheimer’s and Parkinson’s diseases. In the brain, identifying specific phospholipid biomarkers can offer valuable insights into the underlying molecular features and biochemistry of these diseases through a variety of sensitive analytical techniques. Phospholipidomics has emerged as a promising tool in clinical studies, with immense potential to advance our knowledge of neurological diseases and enhance diagnosis and treatment options for patients. In the present review paper, we discussed numerous applications of phospholipidomics tools in clinical studies, with a particular focus on the neurological field. By exploring phospholipids’ functions in neurological diseases and the potential of phospholipidomics in clinical research, we provided valuable insights that could aid researchers and clinicians in harnessing the full prospective of this innovative practice and improve patient outcomes by providing more potent treatments for neurological diseases.

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          Most cited references190

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          LMSD: LIPID MAPS structure database

          The LIPID MAPS Structure Database (LMSD) is a relational database encompassing structures and annotations of biologically relevant lipids. Structures of lipids in the database come from four sources: (i) LIPID MAPS Consortium's core laboratories and partners; (ii) lipids identified by LIPID MAPS experiments; (iii) computationally generated structures for appropriate lipid classes; (iv) biologically relevant lipids manually curated from LIPID BANK, LIPIDAT and other public sources. All the lipid structures in LMSD are drawn in a consistent fashion. In addition to a classification-based retrieval of lipids, users can search LMSD using either text-based or structure-based search options. The text-based search implementation supports data retrieval by any combination of these data fields: LIPID MAPS ID, systematic or common name, mass, formula, category, main class, and subclass data fields. The structure-based search, in conjunction with optional data fields, provides the capability to perform a substructure search or exact match for the structure drawn by the user. Search results, in addition to structure and annotations, also include relevant links to external databases. The LMSD is publicly available at
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            The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics.

            The amyloid cascade hypothesis, which posits that the deposition of the amyloid-β peptide in the brain is a central event in Alzheimer's disease pathology, has dominated research for the past twenty years. Several therapeutics that were purported to reduce amyloid-β production or aggregation have failed in Phase III clinical testing, and many others are in various stages of development. Therefore, it is timely to review the science underpinning the amyloid cascade hypothesis, consider what type of clinical trials will constitute a valid test of this hypothesis and explore whether amyloid-β-directed therapeutics will provide the medicines that are urgently needed by society for treating this devastating disease.
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              A role for docosahexaenoic acid-derived neuroprotectin D1 in neural cell survival and Alzheimer disease.

              Deficiency in docosahexaenoic acid (DHA), a brain-essential omega-3 fatty acid, is associated with cognitive decline. Here we report that, in cytokine-stressed human neural cells, DHA attenuates amyloid-beta (Abeta) secretion, an effect accompanied by the formation of NPD1, a novel, DHA-derived 10,17S-docosatriene. DHA and NPD1 were reduced in Alzheimer disease (AD) hippocampal cornu ammonis region 1, but not in the thalamus or occipital lobes from the same brains. The expression of key enzymes in NPD1 biosynthesis, cytosolic phospholipase A2 and 15-lipoxygenase, was altered in AD hippocampus. NPD1 repressed Abeta42-triggered activation of proinflammatory genes while upregulating the antiapoptotic genes encoding Bcl-2, Bcl-xl, and Bfl-1(A1). Soluble amyloid precursor protein-alpha stimulated NPD1 biosynthesis from DHA. These results indicate that NPD1 promotes brain cell survival via the induction of antiapoptotic and neuroprotective gene-expression programs that suppress Abeta42-induced neurotoxicity.
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                Author and article information

                Contributors
                mayssa.hachem@ku.ac.ae
                Journal
                Mol Neurobiol
                Mol Neurobiol
                Molecular Neurobiology
                Springer US (New York )
                0893-7648
                1559-1182
                20 November 2023
                20 November 2023
                2024
                : 61
                : 6
                : 3272-3295
                Affiliations
                [1 ]Department of Chemistry and Healthcare Engineering Innovation Center, Khalifa University of Sciences and Technology, ( https://ror.org/05hffr360) P.O. Box 127788, Abu Dhabi, United Arab Emirates
                [2 ]Department of Fishing and Post-Harvest Technology, Chattogram Veterinary and Animal Sciences University, ( https://ror.org/045v4z873) Chattogram, Bangladesh
                [3 ]GRID grid.484608.6, ISNI 0000 0004 7661 6266, Riddet Institute, Massey University, ; Palmerston North, New Zealand
                [4 ]Department of Chemistry, Khalifa University of Sciences and Technology, ( https://ror.org/05hffr360) P.O. Box 127788, Abu Dhabi, United Arab Emirates
                Author information
                http://orcid.org/0000-0003-1986-8304
                Article
                3793
                10.1007/s12035-023-03793-y
                11087356
                37981628
                f2b445b5-a8f4-46b5-b9aa-1e909f7175db
                © The Author(s) 2023

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 19 May 2023
                : 31 October 2023
                Categories
                Article
                Custom metadata
                © Springer Science+Business Media, LLC, part of Springer Nature 2024

                Neurosciences
                lipidomics,brain lipid,lipid profiling,lipid biomarkers,analytical approaches,clinical trials

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