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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
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Controlled Cortical Impact Model for Traumatic Brain Injury
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Amlexanox Ameliorates Traumatic Brain Injury by Restoring Autophagy-Lysosomal Function via cAMP Signaling Modulation.

Seo Young Woo1, Min Kyu Park1, A Ra Kho2,3

  • 1Department of Physiology, Hallym University College of Medicine, Chuncheon 24252, Republic of Korea.

International Journal of Biological Sciences
|August 6, 2025
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Summary

Amlexanox (AMX) shows promise for treating traumatic brain injury (TBI). This phosphodiesterase inhibitor restores lysosomal function and reduces neuroinflammation, improving cognitive deficits after TBI.

Keywords:
amlexanox (AMX)autophagycyclic adenosine monophosphate (cAMP)lysosomal dysfunctionneuronal deathphosphodiesterase (PDE)protein kinase A (PKA)traumatic brain injury (TBI)

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Cell Biology

Background:

  • Traumatic brain injury (TBI) causes neuronal damage via lysosomal dysfunction, oxidative stress, and impaired autophagy.
  • Current therapeutic options for TBI are limited, necessitating novel treatment strategies.

Purpose of the Study:

  • To investigate amlexanox (AMX), a phosphodiesterase (PDE) inhibitor, as a potential therapeutic agent for TBI.
  • To elucidate the mechanisms underlying AMX's effects on TBI-induced neuronal damage.

Main Methods:

  • High-throughput screening identified AMX for its ability to restore lysosomal acidity via protein kinase A (PKA) activation.
  • In vitro assays assessed AMX's effects on lysosomal function, dendritic loss, and neuronal survival.
  • In vivo studies utilized a controlled cortical impact model to evaluate AMX's impact on oxidative stress, neuroinflammation, and neuronal viability.
  • Behavioral assessments measured cognitive and neurological function post-TBI.

Main Results:

  • AMX restored lysosomal acidity and enhanced lysosomal function in neuronal cultures.
  • In vivo, AMX reduced oxidative stress, endoplasmic reticulum stress, and neuroinflammation (microglial and astrocytic activation).
  • AMX preserved hippocampal neuronal viability and significantly improved cognitive and neurological deficits in TBI models.

Conclusions:

  • Amlexanox (AMX) demonstrates significant therapeutic potential for traumatic brain injury (TBI).
  • AMX mitigates TBI-induced neuronal damage by restoring lysosomal function and exerting anti-inflammatory effects.
  • The multi-target inhibition of PDEs and modulation of inflammatory pathways underpin AMX's neuroprotective actions.