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URB597 improves cognitive impairment induced by chronic cerebral hypoperfusion by inhibiting mTOR-dependent autophagy

Dapeng Wang1, Qi Lin2, Shaohua Su1

  • 1Department of Neurosurgery, Tong Ji Hospital, Tong Ji University School of Medicine, Shanghai 200065, China.

Neuroscience
|January 3, 2017
PubMed

Insights

The fatty acid amide hydrolase (FAAH) inhibitor URB597 improves cognitive function in chronic cerebral hypoperfusion models by reducing autophagy via mTOR signaling, mitigating neuronal damage.

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Pharmacology

Background:

  • Chronic cerebral hypoperfusion (CCH) is linked to cognitive impairment in ischemic cerebrovascular diseases.
  • The specific role of autophagy in CCH-induced cognitive dysfunction remains unclear.

Purpose of the Study:

  • To investigate the effects of the fatty acid amide hydrolase (FAAH) inhibitor URB597 on autophagy and cognitive function in a CCH model.
  • To elucidate the underlying mechanisms, including the mammalian target of rapamycin (mTOR) signaling pathway.

Main Methods:

  • Morris water maze and long-term potentiation (LTP) for cognitive function assessment.
  • Immunofluorescence, western blot, and transmission electron microscopy (EM) for evaluating autophagy proteins, mTOR signaling, and ultrastructural changes.

Main Results:

  • URB597 treatment improved cognitive impairment in the CCH model.
  • URB597 inhibited CCH-induced autophagy, correlating with modulation of mTOR signaling.
  • Chronic URB597 administration ameliorated CCH-induced ultrastructural neuronal damage.

Conclusions:

  • URB597 modulates autophagy in an mTOR-dependent manner.
  • URB597 mitigates neuronal damage and cognitive deterioration associated with CCH.

Keywords:
autophagychronic cerebral hypoperfusioncognitive impairmentendocannabinoid systemmTOR signaling

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