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Biomolecules
Special Issues
Lipid Signaling in Neuroinflammation and Neurodegeneration
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Lipid Signaling in Neuroinflammation and Neurodegeneration

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: 20 January 2026 | Viewed by 1290

Special Issue Editor

Dr. Jason R. Gerstner

E-Mail Website
Guest Editor
1. Elson S. Floyd College of Medicine, Washington State University, Spokane, WA 99202, USA
2. Steve Gleason Institute for Neuroscience, Washington State University, Spokane, WA 99202, USA
Interests: molecular mechanisms; sleep; circadian rhythms; lipid signaling; neuroinflammation; neurodegenerative disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will explore the crucial role played by lipid signaling pathways in the mechanisms underlying neuroinflammation and neurodegenerative diseases. Lipids are essential biological molecules that serve not only as structural components of cell membranes but also as active signaling mediators influencing numerous neural processes. Alterations in lipid metabolism and signaling have been linked to various neurodegenerative conditions, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS). Understanding how lipid-derived mediators such as sphingolipids, phospholipids, eicosanoids, and endocannabinoids regulate neuroinflammatory responses will open up promising avenues for novel therapeutic strategies. This Special Issue will elucidate the molecular mechanisms through which lipid signaling modulates neural inflammation and cell survival and death, providing insights into potential lipid-based biomarkers and drug targets. Interdisciplinary research combining biochemistry, neurobiology, and molecular biology is central in advancing our knowledge of lipid functions in the diseased brain. By consolidating recent findings, this Special Issue will foster a comprehensive understanding of the influence of lipid signaling in neuroinflammation and neurodegeneration, ultimately contributing to the development of better diagnostic and therapeutic approaches.

Dr. Jason R. Gerstner
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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • lipid signaling
  • neuroinflammation
  • neurodegeneration
  • sphingolipids
  • eicosanoids
  • phospholipids
  • endocannabinoids
  • lipid mediators
  • molecular mechanisms
  • brain health

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Published Papers (2 papers)

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20 pages, 3602 KB  
Article
Kaempferol Regulates Lipid Homeostasis, Endocannabinoid System, and PPARα in Rat Cerebral Cortex Following BCCAO/R
by Gianfranca Carta, Maria Pina Serra, Elisabetta Murru, Marianna Boi, Claudia Manca, Ylenia Lai, Monica Cabboi, Antonella Carta, Sebastiano Banni and Marina Quartu
Biomolecules 2025, 15(10), 1440; https://doi.org/10.3390/biom15101440 - 11 Oct 2025
Viewed by 418
Abstract
Previous research has demonstrated that the transient bilateral common carotid artery occlusion and reperfusion (BCCAO/R) effectively models early brain inflammation resulting from sudden hypoperfusion and subsequent reperfusion. According to studies showing that diet and nutrition strongly influence brain neuroplasticity, in this study we [...] Read more.
Previous research has demonstrated that the transient bilateral common carotid artery occlusion and reperfusion (BCCAO/R) effectively models early brain inflammation resulting from sudden hypoperfusion and subsequent reperfusion. According to studies showing that diet and nutrition strongly influence brain neuroplasticity, in this study we evaluated whether kaempferol (KAM), a dietary flavonoid, offers neuroprotection in a rat BCCAO/R model. Adult Wistar rats were gavage fed a single dose of KAM (40 mg) six hours before surgery. Comprehensive lipidomic and molecular analyses were conducted on samples from the frontal and temporal-occipital cortices, as well as the plasma. In the frontal cortex, KAM elevated anti-inflammatory N-acylethanolamines palmitoylethanolamide (PEA), oleoylethanolamide (OEA), and docosahexaenoylethanolamide (DHAEA) and reduced oxidized arachidonic acid metabolites. KAM also downregulated cyclooxygenase- 2 (COX-2) protein and selectively decreased the endocannabinoid 2-arachidonoylglycerol (2-AG), showing a shift in AA metabolism. These molecular changes correlated with increased levels of peroxisome proliferator-activated receptor alpha (PPARα) and cannabinoid receptors CB1R and CB2R, supporting activation of both nuclear and membrane-bound anti-inflammatory pathways. No significant changes were observed in the temporal-occipital cortex. In plasma, DHAEA levels increased similarly to those in the cortex. However, rises in PEA and OEA were detected only in sham-operated KAM-treated animals, suggesting possible central redistribution under hypoperfusion/reperfusion stress. In summary, these findings demonstrate that KAM exerts dual anti-inflammatory effects by inhibiting COX-2-mediated prostanoid synthesis and promoting PPARα-driven lipid signaling. This dual mechanism highlights the potential of KAM as a dietary intervention to reduce neuroinflammation associated with hypoperfusion–reperfusion challenges. Full article
(This article belongs to the Special Issue Lipid Signaling in Neuroinflammation and Neurodegeneration)
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Other

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13 pages, 1781 KB  
Perspective
A Neural-Glial Model of the ApoE-SORT1-FABP7 Axis Tied to Sleep Disruption and Alzheimer’s Disease Pathophysiology
by Carlos C. Flores, Yool Lee, Christopher J. Davis, Patrick Solverson and Jason R. Gerstner
Biomolecules 2025, 15(10), 1432; https://doi.org/10.3390/biom15101432 - 10 Oct 2025
Viewed by 658
Abstract
Alzheimer’s disease (AD) is a complex neurodegenerative disorder where age, genetic factors and sleep disturbance significantly influence disease risk. Recent genome-wide association studies identified a C/T missense variant (rs141749679) in the sortilin (SORT1) gene linked to heightened AD risk, revealing SORT1’s [...] Read more.
Alzheimer’s disease (AD) is a complex neurodegenerative disorder where age, genetic factors and sleep disturbance significantly influence disease risk. Recent genome-wide association studies identified a C/T missense variant (rs141749679) in the sortilin (SORT1) gene linked to heightened AD risk, revealing SORT1’s role as a key player in the disease’s pathophysiology. This type I membrane glycoprotein is implicated in amyloid β (Aβ) accumulation and associated lipid dysregulation, particularly through its interaction with apolipoprotein E (ApoE). SORT1 facilitates the uptake of ApoE-bound polyunsaturated fatty acids (PUFAs), conversion to endocannabinoids (eCBs), and the regulation of anti-inflammatory pathways via peroxisome proliferator-activated receptors (PPARs). Notably, this neuroprotective signaling is contingent on the APOE allele, exhibiting functionality in presence of ApoE3 but disrupted with ApoE4. Additionally, the brain-type fatty acid binding protein, FABP7, mediates this signaling cascade, emphasizing its role in neuron-glia communication. FABP7 is known to regulate sleep across species and binds PUFAs and eCBs. Therefore, dysfunction of the ApoE-SORT1-FABP7 axis may underlie the neuroprotective loss observed in AD, linking sleep disruption and lipid homeostasis to disease progression. This perspective aims to elucidate the intricate neural-glial mechanisms governing the ApoE-SORT1-FABP7 interaction and their implications for targeting therapeutic interventions in Alzheimer’s disease. Full article
(This article belongs to the Special Issue Lipid Signaling in Neuroinflammation and Neurodegeneration)
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