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Related Concept Videos

Alzheimer's Disease: Overview01:26

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Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder
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Ethanol Alters APP Processing and Aggravates Alzheimer-Associated Phenotypes.

Daochao Huang1, Mengjiao Yu1, Shou Yang1

  • 1Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.

Molecular Neurobiology
|August 12, 2017
PubMed
Summary

Excessive alcohol consumption, specifically ethanol, accelerates Alzheimer's disease (AD) progression. This study found ethanol increases amyloid-beta production and plaque formation, worsening cognitive decline in AD models.

Keywords:
APP processingAlzheimer’s diseaseAβBACE1Cognitive deficitsEthanol exposure

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Alzheimer's disease (AD) pathogenesis is not fully understood, particularly the role of dietary factors.
  • Excessive alcohol intake is a potential risk factor for AD, but its precise effects remain unclear.

Purpose of the Study:

  • To investigate the relationship between ethanol exposure and Alzheimer's disease development.
  • To determine how ethanol affects amyloid precursor protein (APP) processing and amyloid-beta (Aβ) production.

Main Methods:

  • Exposing cell cultures to ethanol at varying concentrations and durations.
  • Administering ethanol to a transgenic mouse model of Alzheimer's disease for four weeks.
  • Analyzing changes in APP processing, BACE1 levels, Aβ production, plaque formation, and cognitive function.

Main Results:

  • Ethanol exposure altered APP processing, increasing APP and BACE1 levels in cells and AD model mice.
  • High ethanol intake significantly promoted Aβ production both in vitro and in vivo.
  • Ethanol treatment led to increased Aβ deposition, neuritic plaque formation, and exacerbated learning and memory impairments in AD mice.

Conclusions:

  • Excessive ethanol intake facilitates Alzheimer's disease pathogenesis.
  • Ethanol upregulates APP and BACE1 expression, at least partially through transcriptional activation.
  • Ethanol exacerbates key pathological hallmarks and cognitive deficits associated with Alzheimer's disease.