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Volume 10
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10.3390/biomedicines10061236
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Article

Co-Ultramicronized Palmitoylethanolamide/Luteolin Restores Oligodendrocyte Homeostasis via Peroxisome Proliferator-Activated Receptor-α in an In Vitro Model of Alzheimer’s Disease

by
Roberta Facchinetti
1,†,
Marta Valenza
1,†,
Chiara Gomiero
2,
Giulia Federica Mancini
1,3,
Luca Steardo
1,4,
Patrizia Campolongo
1,3 and
Caterina Scuderi
1,*
1
Department of Physiology and Pharmacology “Vittorio Erspamer”, SAPIENZA University of Rome—P. le Aldo Moro, 5, 00185 Rome, Italy
2
Epitech Research Group, 35030 Padova, Italy
3
Centro Europeo di Ricerca sul Cervello (CERC), IRCCS Santa Lucia Foundation Rome, 00143 Rome, Italy
4
Università Telematica Giustino Fortunato, 82100 Benevento, Italy
*
Author to whom correspondence should be addressed.
†
These authors have contributed equally to the work.
Biomedicines 2022, 10(6), 1236; https://doi.org/10.3390/biomedicines10061236
Submission received: 29 April 2022 / Revised: 24 May 2022 / Accepted: 25 May 2022 / Published: 26 May 2022
(This article belongs to the Special Issue Molecular Determinants of Neurodegenerative Diseases)
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Abstract

Oligodendrocytes are cells fundamental for brain functions as they form the myelin sheath and feed axons. They perform these critical functions thanks to the cooperation with other glial cells, mainly astrocytes. The astrocyte/oligodendrocyte crosstalk needs numerous mediators and receptors, such as peroxisome proliferator-activated receptors (PPARs). PPAR agonists promote oligodendrocyte precursor cells (OPCs) maturation in myelinating oligodendrocytes. In the Alzheimer’s disease brain, deposition of beta-amyloid (Aβ) has been linked to several alterations, including astrogliosis and changes in OPCs maturation. However, very little is known about the molecular mechanisms. Here, we investigated for the first time the maturation of OPCs co-cultured with astrocytes in an in vitro model of Aβ1–42 toxicity. We also tested the potential beneficial effect of the anti-inflammatory and neuroprotective composite palmitoylethanolamide and luteolin (co-ultra PEALut), which is known to engage the isoform alfa of the PPARs. Our results show that Aβ1–42 triggers astrocyte reactivity and inflammation and reduces the levels of growth factors important for OPCs maturation. Oligodendrocytes indeed show low cell surface area and few arborizations. Co-ultra PEALut counteracts the Aβ1–42-induced inflammation and astrocyte reactivity preserving the morphology of co-cultured oligodendrocytes through a mechanism that in some cases involves PPAR-α. This is the first evidence of the negative effects exerted by Aβ1–42 on astrocyte/oligodendrocyte crosstalk and discloses a never-explored co-ultra PEALut ability in restoring oligodendrocyte homeostasis.
Keywords: oligodendrocytes; astrocytes; beta-amyloid; palmitoylethanolamide; luteolin; neuroinflammation; peroxisome proliferator-activated receptors; Alzheimer’s disease oligodendrocytes; astrocytes; beta-amyloid; palmitoylethanolamide; luteolin; neuroinflammation; peroxisome proliferator-activated receptors; Alzheimer’s disease

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MDPI and ACS Style

Facchinetti, R.; Valenza, M.; Gomiero, C.; Mancini, G.F.; Steardo, L.; Campolongo, P.; Scuderi, C. Co-Ultramicronized Palmitoylethanolamide/Luteolin Restores Oligodendrocyte Homeostasis via Peroxisome Proliferator-Activated Receptor-α in an In Vitro Model of Alzheimer’s Disease. Biomedicines 2022, 10, 1236. https://doi.org/10.3390/biomedicines10061236

AMA Style

Facchinetti R, Valenza M, Gomiero C, Mancini GF, Steardo L, Campolongo P, Scuderi C. Co-Ultramicronized Palmitoylethanolamide/Luteolin Restores Oligodendrocyte Homeostasis via Peroxisome Proliferator-Activated Receptor-α in an In Vitro Model of Alzheimer’s Disease. Biomedicines. 2022; 10(6):1236. https://doi.org/10.3390/biomedicines10061236

Chicago/Turabian Style

Facchinetti, Roberta, Marta Valenza, Chiara Gomiero, Giulia Federica Mancini, Luca Steardo, Patrizia Campolongo, and Caterina Scuderi. 2022. "Co-Ultramicronized Palmitoylethanolamide/Luteolin Restores Oligodendrocyte Homeostasis via Peroxisome Proliferator-Activated Receptor-α in an In Vitro Model of Alzheimer’s Disease" Biomedicines 10, no. 6: 1236. https://doi.org/10.3390/biomedicines10061236

APA Style

Facchinetti, R., Valenza, M., Gomiero, C., Mancini, G. F., Steardo, L., Campolongo, P., & Scuderi, C. (2022). Co-Ultramicronized Palmitoylethanolamide/Luteolin Restores Oligodendrocyte Homeostasis via Peroxisome Proliferator-Activated Receptor-α in an In Vitro Model of Alzheimer’s Disease. Biomedicines, 10(6), 1236. https://doi.org/10.3390/biomedicines10061236

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