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Molecular Mechanism and Pharmacological Target of Neuroprotection

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (20 April 2026) | Viewed by 603

Special Issue Editor


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Guest Editor
Department of Biological, Geological and Environmental Sciences (BIGEA), University of Bologna, 40126 Bologna, Italy
Interests: zebrafish; neurological disorders; hematopoiesis; brain development; microglia

Special Issue Information

Dear Colleagues,

Neurodegeneration is caused by the progressive loss of neurons and can affect the central and peripheral nervous systems of millions of people worldwide. Many of these disorders can be caused by the alteration of genetic and molecular factors. These defects can induce a progressive decline in memory, locomotion, sensory perception, etc. Although considerable discoveries have been achieved by researchers worldwide, the pathogenesis of neurodegeneration is still unclear, and no pharmacological strategies or drugs can stop or alleviate progressive neurodegeneration in the brains and spinal cords of affected patients.

This Special Issue will focus on the molecular mechanisms and pharmacological targets of neuroprotection. Novel findings on key pharmacological targets and underlying molecular mechanisms will help us to develop new therapeutic strategies and agents to treat neurodegeneration. In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Use of in vitro or in vivo models to identify new pharmacological neuroprotectors;
  • Use and/or generation of animal models to study neurodegeneration;
  • Identifying specific molecular targets to induce neural repair.

Dr. Pietro Cacialli
Guest Editor

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Keywords

  • neurodegeneration
  • animal model
  • brain regeneration
  • pharmacological drug
  • molecular analysis

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Published Papers (1 paper)

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Research

20 pages, 4841 KB  
Article
Central Administration of Recombinant IGF1 Is Neuroprotective in a Rodent Model of Acute Liver Failure
by Yubo Wang, Matthew McMillin, Gabriel Frampton, Kathryn Rhodes, Elaina Williams, Juliet Venter, Jace Tyson, Esha Gupta, Mihika Patankar, Patrick Mireles and Sharon DeMorrow
Int. J. Mol. Sci. 2026, 27(8), 3547; https://doi.org/10.3390/ijms27083547 - 16 Apr 2026
Viewed by 269
Abstract
Acute liver failure is often accompanied by neurological disturbances collectively referred to as hepatic encephalopathy (HE), characterized by neuroinflammation and subsequent cognitive decline. Insulin-like growth factor 1 (IGF1) is a neuroprotective peptide with anti-inflammatory properties in the brain. The role of IGF1 in [...] Read more.
Acute liver failure is often accompanied by neurological disturbances collectively referred to as hepatic encephalopathy (HE), characterized by neuroinflammation and subsequent cognitive decline. Insulin-like growth factor 1 (IGF1) is a neuroprotective peptide with anti-inflammatory properties in the brain. The role of IGF1 in cognitive deficits and neuroinflammation during HE remains largely unexplored. In C57Bl/6 mice, HE was established through an intraperitoneal injection of azoxymethane (AOM), and tissues were collected at defined time points during disease development. IGF1 expression in the cortex was downregulated following AOM administration. Central infusion of recombinant mouse IGF1 (rmIGF1) before AOM injection resulted in delayed neurological impairment, reduced microglial activation, and decreased proinflammatory cytokine and chemokine production in AOM mice. In vitro, rmIGF1 and conditioned media derived from rmIGF1-treated primary neurons attenuated phagocytic activity and C–C motif chemokine ligand 2 (CCL2) production in the microglial cell line EOC-20. Collectively, our results show that IGF1, whose levels decline during HE, alleviates neuroinflammation and improves the pathological state of AOM-treated mice through the suppression of microglial activation and the regulation of neuron–microglia paracrine communication. Full article
(This article belongs to the Special Issue Molecular Mechanism and Pharmacological Target of Neuroprotection)
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