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Biomolecules
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Targeting Neuroinflammation and Insulin Resistance for a Healthy Brain: Prevention...
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Targeting Neuroinflammation and Insulin Resistance for a Healthy Brain: Prevention and Treatment of Neurological and Psychiatric Disorders

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 1511

Special Issue Editors

Prof. Dr. Ana María Sánchez-Pérez

E-Mail Website
Guest Editor
Faculty of Health Science and Institute of Advanced Materials (INAM), University Jaume I, 12071 Castellon, Spain
Interests: neuroinflammation; psychiatric disorders; insulin resistance; chitosan nanoparticles; AAV particles; non-coding RNA; animal models; cell culture
Special Issues, Collections and Topics in MDPI journals
Dr. Sandra Sánchez-Sarasúa

E-Mail Website
Guest Editor
Team "Purinergic-Mediated Neuroinflammation and Brain Disorders", Institut des Maladies Neurodégénératives IMN (CNRS UMR 5293), Centre Broca Nouvelle Aquitaine, Université de Bordeaux, 33000 Bordeaux, France
Interests: neuroscience; brain circuits; behaviour; cell culture; western blot; immunohistochemistry; insulin resistance; neuroinflammation; ADHD; learning and memory; microscopy

Special Issue Information

Dear Colleagues,

Neuroinflammation and insulin resistance form a bidirectional process that induces neuronal damage. Inflammatory events and insulin resistance have been associated with the onset of neurodegenerative pathologies, including late-onset Alzheimer’s disease and Parkinson’s disease. Accumulating evidence indicates that neuroinflammation and insulin resistance can also underlie psychiatric disorders. Several conditions, ranging from emotional stress to metabolic syndrome, including traumatic brain injury, chronic infections, or gut dysbiosis, can cause or aggravate insulin resistance and neuroinflammation.

The Western lifestyle is characterized by stress, sedentarism, and high caloric intake, which increases the risk of suffering from diverse brain disorders. Interventions that reduce neuroinflammation and improve insulin signaling (i.e., physical exercise, nutrition supplementation) can improve synaptic plasticity and brain cognitive function.

Review articles and original research papers, showing novel mechanisms underlying the association of neuroinflammation and brain insulin resistance with brain dysfunction and showing evidence of novel biomarkers or genetic predisposition are welcome. We invite contributions raising the knowledge and awareness of the need for early intervention in controlling neuroinflammation and insulin resistance to improve neurological and psychiatric disorders’ management.

Dr. Ana María Sánchez-Pérez
Dr. Sandra Sánchez-Sarasúa
Guest Editors

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

  • insulin receptor substrates
  • microglia
  • degenerative diseases
  • psychiatric disorders
  • nutrition

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Published Papers (1 paper)

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Research

28 pages, 4760 KiB  
Article
Single-Cell RNA Sequencing Reveals Immunomodulatory Effects of Stem Cell Factor and Granulocyte Colony-Stimulating Factor Treatment in the Brains of Aged APP/PS1 Mice
by Robert S. Gardner, Michele Kyle, Karen Hughes and Li-Ru Zhao
Biomolecules 2024, 14(7), 827; https://doi.org/10.3390/biom14070827 - 10 Jul 2024
Viewed by 828
Abstract
Alzheimer’s disease (AD) leads to progressive neurodegeneration and dementia. AD primarily affects older adults with neuropathological changes including amyloid-beta (Aβ) deposition, neuroinflammation, and neurodegeneration. We have previously demonstrated that systemic treatment with combined stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) (SCF+G-CSF) [...] Read more.
Alzheimer’s disease (AD) leads to progressive neurodegeneration and dementia. AD primarily affects older adults with neuropathological changes including amyloid-beta (Aβ) deposition, neuroinflammation, and neurodegeneration. We have previously demonstrated that systemic treatment with combined stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) (SCF+G-CSF) reduces the Aβ load, increases Aβ uptake by activated microglia and macrophages, reduces neuroinflammation, and restores dendrites and synapses in the brains of aged APPswe/PS1dE9 (APP/PS1) mice. However, the mechanisms underlying SCF+G-CSF-enhanced brain repair in aged APP/PS1 mice remain unclear. This study used a transcriptomic approach to identify the potential mechanisms by which SCF+G-CSF treatment modulates microglia and peripheral myeloid cells to mitigate AD pathology in the aged brain. After injections of SCF+G-CSF for 5 consecutive days, single-cell RNA sequencing was performed on CD11b+ cells isolated from the brains of 28-month-old APP/PS1 mice. The vast majority of cell clusters aligned with transcriptional profiles of microglia in various activation states. However, SCF+G-CSF treatment dramatically increased a cell population showing upregulation of marker genes related to peripheral myeloid cells. Flow cytometry data also revealed an SCF+G-CSF-induced increase of cerebral CD45high/CD11b+ active phagocytes. SCF+G-CSF treatment robustly increased the transcription of genes implicated in immune cell activation, including gene sets that regulate inflammatory processes and cell migration. The expression of S100a8 and S100a9 was robustly enhanced following SCF+G-CSF treatment in all CD11b+ cell clusters. Moreover, the topmost genes differentially expressed with SCF+G-CSF treatment were largely upregulated in S100a8/9-positive cells, suggesting a well-conserved transcriptional profile related to SCF+G-CSF treatment in resident and peripherally derived CD11b+ immune cells. This S100a8/9-associated transcriptional profile contained notable genes related to pro-inflammatory and anti-inflammatory responses, neuroprotection, and Aβ plaque inhibition or clearance. Altogether, this study reveals the immunomodulatory effects of SCF+G-CSF treatment in the aged brain with AD pathology, which will guide future studies to further uncover the therapeutic mechanisms. Full article
(This article belongs to the Special Issue Targeting Neuroinflammation and Insulin Resistance for a Healthy Brain: Prevention and Treatment of Neurological and Psychiatric Disorders)
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