Journal Article

DZNE-2025-00010

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png The Neuroprotective Effects of Caffeine in a Neonatal Hypoxia-Ischemia Model are Regulated through the AMPK/mTOR Pathway.

Bernis, M. E. (First author)DZNE* ; Burkard, H.DZNE* ; Bremer, A.-S.DZNE* ; Grzelak, K.DZNE* ; Zweyer, M.DZNE* ; Maes, E.DZNE* ; Nacarkucuk, E.Extern* ; Kaibel, H.Extern* ; Hakvoort, C.Extern* ; Müller, A. ; Sabir, H. (Last author)DZNE*

2025
Ivyspring International Publ. Lake Haven, N.S.W. [u.a.]

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Please use a persistent id in citations: doi:10.7150/ijbs.101087

Abstract: Neonatal hypoxic-ischemic encephalopathy (HIE) is the most common cause of death and long-term disabilities in term neonates. Caffeine exerts anti-inflammatory effects and has been used in neonatal intensive care units in recent decades. In our neonatal rat model of hypoxic-ischemic (HI) brain injury, we demonstrated that a single daily dose of caffeine (40 mg/kg) for 3 days post-HI reduced brain tissue loss and microgliosis compared to the vehicle group. The AMPK/mTOR pathway plays an important role in sensing the stress responses following brain injury. However, the role of mTOR in HI-associated brain damage remains unclear. A detailed analysis of the AMPK/mTOR pathway in our model revealed that this pathway plays a key role in hypoxia-regulated neuroprotection and can be significantly influenced by caffeine treatment. Targeting HI with caffeine might offer effective neuroprotection, reduce mortality, and improve functional outcomes in patients with HIE, especially in low- and middle-income countries, where neuroprotective treatment is urgently needed.

Keyword(s): Caffeine: pharmacology (MeSH) ; Caffeine: therapeutic use (MeSH) ; Animals (MeSH) ; Neuroprotective Agents: therapeutic use (MeSH) ; Neuroprotective Agents: pharmacology (MeSH) ; TOR Serine-Threonine Kinases: metabolism (MeSH) ; Hypoxia-Ischemia, Brain: metabolism (MeSH) ; Hypoxia-Ischemia, Brain: drug therapy (MeSH) ; Rats (MeSH) ; Animals, Newborn (MeSH) ; Rats, Sprague-Dawley (MeSH) ; AMP-Activated Protein Kinases: metabolism (MeSH) ; Signal Transduction: drug effects (MeSH) ; Disease Models, Animal (MeSH) ; AMPK ; Caffeine ; Hypoxia-Ischemia ; Neonatal ; Neuroprotection ; mTOR ; Caffeine ; Neuroprotective Agents ; TOR Serine-Threonine Kinases ; AMP-Activated Protein Kinases

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Contributing Institute(s):

1. Neonatal Neuroscience (AG Sabir)
2. Nuclear Function in CNS Pathophysiology (AG Salomoni)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)

Appears in the scientific report 2025

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