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Related Concept Videos

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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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FAAH Inhibition Counteracts Neuroinflammation via Autophagy Recovery in AD Models.

Federica Armeli1, Roberto Coccurello2,3, Giacomo Giacovazzo2,4

  • 1Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, 04100 Latina, Italy.

International Journal of Molecular Sciences
|November 27, 2024
PubMed
Summary

Increasing endocannabinoid levels with URB597 reduced Alzheimer

Keywords:
ATG7Alzheimer’s disease (AD)BDNFURB597autophagyendocannabinoidsfatty acid amide hydrolasemTORmicroglianeuroinflammation

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Neuroinflammation is a key feature of Alzheimer's disease (AD).
  • Endocannabinoids show potential in counteracting neuroinflammation.
  • Autophagic mechanisms may be involved in AD pathogenesis.

Purpose of the Study:

  • To investigate if increasing endocannabinoid tone via URB597 rebalances autophagic mechanisms in cellular and animal models of AD.
  • To evaluate the therapeutic potential of URB597 in reducing AD pathology.

Main Methods:

  • Utilized microglial cultures treated with amyloid-beta (Aβ25-35) and Tg2576 transgenic mice.
  • Administered URB597, a Fatty-Acid Amide Hydrolase (FAAH) inhibitor, to increase anandamide levels.
  • Assessed microglia polarization, cytokine expression, amyloid plaque load, and autophagy markers (BECN1, ATG7, LC3, SQSTM1/p62, ULK1 pathway).

Main Results:

  • URB597 treatment polarized microglia towards an anti-inflammatory phenotype, increasing BDNF and Nrf2 expression.
  • Amyloid plaque number and area were reduced in URB597-treated mice.
  • Autophagy was restored in Tg2576 mice, evidenced by increased BECN1, ATG7, LC3, SQSTM1/p62, and ULK1 pathway activation.

Conclusions:

  • Increasing endocannabinoid tone with URB597 counteracts neuroinflammation and reduces amyloid pathology in AD models.
  • URB597 rebalances autophagy via the mTOR/ULK1-dependent pathway.
  • Endocannabinoids represent a promising therapeutic strategy for Alzheimer's disease by modulating autophagy.