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Related Concept Videos

Alzheimer's Disease: Treatment01:22

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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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Cracking Amyloid Toxicity: Naringin Rescues Neuronal Cells in a Minimal Alzheimer's Model.

Emre Korkmaz1, Jülide Secerli1, Hakan Erdoğan2

  • 1Gülhane Faculty of Pharmacy, Department of Pharmaceutical Toxicology, University of Health Sciences Turkey, Ankara 06018, Turkey.

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Summary

Naringin (NAR) protects against Alzheimer's disease (AD) by reducing oxidative stress, DNA damage, and inflammation in a novel diphenylalanine-induced cell model. This study highlights NAR's potential as a neuroprotective therapeutic agent for AD.

Keywords:
amyloid plaqueapoptosisdiphenylalanineinflammationneuroprotectionoxidative stress

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is a neurodegenerative disorder marked by cognitive decline and amyloid plaques.
  • Diphenylalanine (Phe-Phe) offers a simplified in vitro model for studying amyloid aggregation relevant to AD.
  • Naringin (NAR), a citrus flavanone, possesses known antioxidant and anti-inflammatory properties.

Purpose of the Study:

  • To investigate the neuroprotective effects of naringin (NAR) in a diphenylalanine (Phe-Phe)-induced Alzheimer's disease (AD) model.
  • To evaluate NAR's impact on oxidative stress, DNA damage, inflammation, and apoptosis in neuroblastoma cells.
  • To assess NAR's influence on key AD biomarkers including acetylcholinesterase (AChE), amyloid beta (Aβ), amyloid precursor protein (APP), and tau protein.

Main Methods:

  • Established a Phe-Phe-induced AD model using SH-SY5Y neuroblastoma cells.
  • Treated Phe-Phe-exposed cells with subcytotoxic concentrations of naringin (NAR).
  • Assessed cytotoxicity, reactive oxygen species (ROS) generation, DNA damage (Comet assay), biomarker levels, cytokine profiles, caspase activation, and apoptosis.

Main Results:

  • NAR treatment significantly reduced Phe-Phe-induced ROS production and genotoxicity.
  • NAR attenuated inflammatory responses and decreased apoptotic cell death in the AD model.
  • NAR effectively restored AD-related biomarker levels (AChE, Aβ, APP, tau) towards normal physiological ranges.

Conclusions:

  • Naringin (NAR) demonstrates multitargeted neuroprotective effects against Alzheimer's disease pathology.
  • The Phe-Phe model serves as a validated in vitro system for screening anti-amyloid agents.
  • Naringin shows therapeutic potential for managing Alzheimer's disease.