Cited by 244Sphingolipid Metabolism and SignalingAlzheimer's disease research and treatmentsLysosomal Storage Disorders Research

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Ceramides in Alzheimer’s Disease: Key Mediators of Neuronal Apoptosis Induced by Oxidative Stress and A β Accumulation

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Jazvinšćak Jembrek, Maja, Hof, Patrick R., Šimić, Goran·2015·Oxidative Medicine and Cellular Longevity

DOI 10.1155/2015/346783PMC PMC4458271

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Abstract

Alzheimer’s disease (AD), the most common chronic and progressive neurodegenerative disorder, is characterized by extracellular deposits of amyloid β -peptides (A β ) and intracellular deposits of hyperphosphorylated tau (phospho-tau) protein. Ceramides, the major molecules of sphingolipid metabolism and lipid second messengers, have been associated with AD progression and pathology via A β generation. Enhanced levels of ceramides directly increase A β through stabilization of β -secretase, the key enzyme in the amyloidogenic processing of A β precursor protein (APP). As a positive feedback loop, the generated oligomeric and fibrillar A β induces a further increase in ceramide levels by activating sphingomyelinases that catalyze the catabolic breakdown of sphingomyelin to ceramide. Evidence also supports important role of ceramides in neuronal apoptosis. Ceramides may initiate a cascade of biochemical alterations, which ultimately leads to neuronal death by diverse mechanisms, including depolarization and permeabilization of mitochondria, increased production of reactive oxygen species (ROS), cytochrome c release, Bcl-2 depletion, and caspase-3 activation, mainly by modulating intracellular signalling, particularly along the pathways related to Akt/PKB kinase and mitogen-activated protein kinases (MAPKs). This review summarizes recent findings related to the role of ceramides in oxidative stress-driven neuronal apoptosis and interplay with A β in the cascade of events ending in neuronal degeneration.

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Authors: Jazvinšćak Jembrek, M., Hof, P. R., & Šimić, G.
Affiliations: Laboratory for Molecular Neuropharmacology, Division of Molecular Medicine, Rudjer Bošković Institute, 10000 Zagreb, Croatia
Icahn School of Medicine at Mount Sinai (US)
University of Zagreb (HR)
ORCID: Hof, Patrick R.
Šimić, Goran
Venue: Oxidative Medicine and Cellular Longevity
Publisher: Wiley
Published: 2015
Volume: 2015
Pages: 1-17
ISSN: 1942-0994 (ISSN-L)
1942-0900
DOI: 10.1155/2015/346783
PMC: PMC4458271
OpenAlex: W1484835368
Cited by: 244
References: 199
Citations by year: 2026: 13 · 2025: 22 · 2024: 26 · 2023: 23 · 2022: 27 · 2021: 29 · 2020: 21 · 2019: 29 · 2018: 20 · 2017: 21 · 2016: 10 · 2015: 3
FWCI: 1.74
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
creativecommons.org/licenses/by/3.0/ (unspecified)
Locations: Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Repository of the Medical Faculty of the University of Zagreb (University of Zagreb) (acceptedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Institutional Repository of the Ruđer Bošković Institute (Ruđer Bošković Institute) (submittedVersion, cc-by)
Institutional Repository of the Ruđer Bošković Institute (Ruđer Bošković Institute) (submittedVersion, other-oa)
Funders: Croatian Ministry of Science, Education and Sport (098-0000000-2448, 09/16, AG005138)
Croatian Science Foundation (098-0000000-2448, 09/16, AG005138)
National Institutes of Health (098-0000000-2448, 09/16, AG005138)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Genetics (clinical) › Lysosomal Storage Disorders Research
Keywords: ceramide, Alzheimer's disease, amyloid-beta, oxidative stress, neuronal apoptosis, sphingolipid metabolism, beta-secretase, sphingomyelinase, tau hyperphosphorylation, mitochondrial membrane permeabilization, reactive oxygen species, caspase-3, Akt signaling, MAPK signaling, neurodegeneration
MeSH terms: Alzheimer Disease, Animals, Ceramides, Humans, Neurons, Amyloid beta-Peptides, Apoptosis, Oxidative Stress

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Ceramides in Alzheimer’s Disease: Key Mediators of Neuronal Apoptosis Induced by Oxidative Stress and A β Accumulation

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