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Basic Science and Pathogenesis.

Ricardo A S Lima-Filho1, Alinny Isaac2, Cristovão De Lanna3

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|December 23, 2025
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Summary
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Low-dose ketamine may alter Alzheimer's disease (AD) risk by inducing AD-like gene expression changes in the brain. Caution is advised when using ketamine in AD patients or those at risk.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Genetics

Background:

  • Ketamine, an NMDA receptor antagonist, is used for anesthesia and has antidepressant properties.
  • Major depressive disorder (MDD) is linked to Alzheimer's disease (AD), sharing hallmarks like neuroinflammation and synaptic dysfunction.
  • The impact of ketamine on AD pathology remains largely unexplored.

Purpose of the Study:

  • To investigate ketamine's effects on AD pathological markers in mouse models.
  • To evaluate memory, amyloid pathology, and glial changes following ketamine administration.
  • To analyze transcriptomic alterations induced by ketamine in the context of AD.

Main Methods:

  • Administered single-dose ketamine to amyloid-β oligomer (AβO) injected mice.
  • Chronically treated transgenic APP/PS1 mice with ketamine for 35 days.
  • Performed memory tests, immunohistology, and RNA sequencing on mouse hippocampi.

Main Results:

  • Ketamine protected against AβO-induced memory impairment, but chronic treatment showed no memory benefit in APP/PS1 mice.
  • Chronic ketamine induced an AD-like transcriptional profile in wildtype (WT) mice.
  • Ketamine modulated gene expression related to synaptic transmission, protein translation, and glial function, with opposing effects in WT and APP/PS1 mice.

Conclusions:

  • Chronic low-dose ketamine elicits a distinct transcriptional and cellular response in AD models.
  • Ketamine induces an AD-like transcriptional signature in WT mice, suggesting potential modulation of AD risk.
  • Clinical use of low-dose ketamine in individuals at risk for or diagnosed with AD warrants careful consideration.