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Basic Science and Pathogenesis.

Joao D Calixtro1, Felipe C Ribeiro1, Danielle Cozachenco Ferreira2

  • 1Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary
This summary is machine-generated.

The ketamine metabolite HNK rescues key gene expression pathways in aged mice with Alzheimer's disease (AD) pathology. HNK treatment improved mRNA translation and reduced inflammation, offering potential therapeutic benefits for AD.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Hippocampal mRNA translation is vital for memory and impaired in Alzheimer's disease (AD).
  • Amyloid precursor protein (APP) and presenilin 1 (PS1) gene mutations lead to AD pathology.
  • Ketamine metabolite HNK is investigated for its potential to restore cellular functions.

Purpose of the Study:

  • To determine if HNK can rescue transcription profiles related to mRNA translation in aged APP/PS1 mice.
  • To investigate HNK's effects on gene expression in a mouse model of AD.

Main Methods:

  • Aged APP/PS1 mice and wild-type (WT) littermates were treated with HNK or saline.
  • Hippocampal transcriptomic changes were analyzed using RNA-sequencing (RNA-seq).
  • Gene Ontology (GO) and Reactome pathway analyses were performed.

Main Results:

  • HNK treatment corrected upregulated pathways in APP/PS1 mice, including programmed cell death and stress response.
  • Reactome analysis identified rescue of RNA metabolism and translation pathways by HNK.
  • HNK normalized aberrant immune system pathways in APP/PS1 mice.

Conclusions:

  • HNK administration rescues transcriptional programs in aged APP/PS1 mice.
  • These rescued pathways involve inflammation, proteostasis, calcium signaling, and synaptic proteins.
  • HNK shows potential for therapeutic intervention in AD by restoring molecular pathways.