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REVIEW article

Front. Neurosci.

Sec. Translational Neuroscience

This article is part of the Research TopicRecent Advances in Translational Neurovascular and Cerebroprotection ResearchView all 9 articles

Neuritin: A Multifaceted Neuroprotective Factor with Emerging Applications for Neurodegeneration

Provisionally accepted
  • Indiana University School of Medicine, Indianapolis, United States

The final, formatted version of the article will be published soon.

Neuritin is a conserved, activity-regulated gene encoding a glycosylphosphatidylinositol-anchored protein, crucial for neural development, synaptic plasticity, and neuroprotection. Identified via activity-dependent gene screening in the rat hippocampus, neuritin promotes neurite outgrowth, dendritic arborization, and synaptic maturation with neural activity. The protein has a conserved structure across species, featuring a 142-amino acid sequence, an N-terminal signal peptide, and a C-terminal GPI anchor. Neuritin's expression is dynamically regulated through signaling pathways like calcium-dependent mechanisms, N-methyl-D-aspartate/α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, brain derived neurotrophic factor and tropomyosin receptor kinase B signaling. Beyond neurodevelopment, neuritin has therapeutic potential in various conditions: it protects against Alzheimer's disease, supports retinal ganglion cell survival in glaucoma, and maintains cochlear integrity in hearing loss. Neuritin is also promising for recovery post-stroke, in diabetic neuropathy, and in neuropsychiatric disorders. Mechanically, it activates pathways such as insulin receptor-mediated signaling while inhibiting Notch signaling. Recent studies reveal roles in immunoregulation, angiogenesis, and cancer biology, highlighting neuritin as a versatile signaling molecule with broad therapeutic implications. Its neuroprotective, neuroregenerative, and neuromodulatory qualities position it as a candidate for addressing neurodegenerative diseases.

Keywords: Neuritin, Neuroprotection, synaptic plasticity, Retinal Ganglion Cells, neurodegeneration

Received: 03 Sep 2025; Accepted: 03 Nov 2025.

Copyright: © 2025 Sharma and Mongan. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Tasneem Putliwala Sharma, tpsharma@iu.edu

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