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CRY2 mediates the cognitive decline induced by sleep deprivation in 5xFAD mice

Sumei Luo1, Lizhe Guo1, Na Chen1

  • 1Department of Anesthesiology, Xiangya Hospital, Central South University, Changsha, China.

Plos One
|July 16, 2024
PubMed
Abstract

Insights

Sleep deprivation worsens cognitive decline in Alzheimer's disease (AD) mice by upregulating Cryptochrome-2 (CRY2), leading to synaptic dysfunction. Downregulating CRY2 can mitigate these effects.

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Cryptochrome-2 (CRY2) is a core rhythm gene involved in DNA damage repair.
  • The study investigates CRY2's role in sleep deprivation-induced cognitive decline in 5xFAD Alzheimer's disease (AD) mouse models.

Purpose of the Study:

  • To determine if CRY2 mediates cognitive decline caused by sleep deprivation in AD mice.
  • To elucidate the molecular mechanisms underlying CRY2's effect on cognitive function.

Main Methods:

  • Utilized 18F FDG PET-CT to assess brain glucose metabolism after sleep deprivation (SD).
  • Evaluated cognitive function using Morris water maze and Y-maze tests.
  • Manipulated CRY2 levels via lentivirus (overexpression) and siRNA (downregulation) in 5xFAD mice.

Main Results:

  • SD induced cognitive decline and increased CRY2 expression in AD mice.
  • CRY2 overexpression worsened cognitive deficits, while CRY2 downregulation attenuated SD-induced decline.
  • CRY2 reduced CISH expression, inhibiting STAT1 phosphorylation and causing synaptic dysfunction.

Conclusions:

  • Sleep deprivation upregulates CRY2 in the hippocampus of AD mice.
  • This upregulation leads to synaptic dysfunction via decreased CISH-mediated STAT1 phosphorylation.
  • Targeting CRY2 may offer a therapeutic strategy for cognitive decline associated with sleep disturbances in AD.

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