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Related Concept Videos

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

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...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
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Alzheimer's Disease: Overview

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.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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Related Experiment Video

Updated: Jul 2, 2026

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein
08:27

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Published on: July 29, 2018

Ribavirin mitigates Alzheimer's disease model phenotypes by enhancing lysosomal function and suppressing ISR.

Zhicheng Yi1, Zihao Yao1, Fuhao Wang2

  • 1Department of Cell Biology, School of Basic Medical Sciences, Laboratory for Clinical Medicine, Capital Medical University, Beijing 100069, China; Ministry of Education Key Laboratory of Cell Proliferation and Differentiation, School of Life Sciences, Peking University, Beijing 100871, China.

Bioorganic Chemistry
|June 30, 2026
PubMed
Summary

Ribavirin, an antiviral drug, shows promise for Alzheimer's disease (AD). It reduced paralysis and improved learning in AD models by inhibiting amyloid-beta aggregation and enhancing cellular repair mechanisms.

Keywords:
Alzheimer's diseaseAβ aggregationC. elegansISRLysosomeRibavirin

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Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase
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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

Related Experiment Videos

Last Updated: Jul 2, 2026

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein
08:27

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Published on: July 29, 2018

Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase
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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
08:01

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

Area of Science:

  • Neuroscience
  • Pharmacology
  • Genetics

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder with no effective treatments.
  • Amyloid-beta (Aβ) aggregation is a key pathological hallmark of AD.

Purpose of the Study:

  • To investigate the therapeutic potential of ribavirin in Alzheimer's disease models.
  • To elucidate the mechanisms underlying ribavirin's neuroprotective effects.

Main Methods:

  • Utilized transgenic Caenorhabditis elegans (C. elegans) models of AD expressing amyloid-beta.
  • Assessed functional outcomes including paralysis rate and learning capacity.
  • Analyzed Aβ aggregation in vivo and in vitro using biophysical techniques.
  • Investigated molecular mechanisms involving lysosomal activity, integrated stress response (ISR), and AMPK signaling.

Main Results:

  • Ribavirin significantly reduced paralysis and improved learning in Aβ C. elegans models.
  • Demonstrated reduced Aβ aggregation in vivo and inhibited α-helix to β-sheet transition in vitro.
  • Showed ribavirin binds to Aβ1-42 pentamers, disrupts β-sheet structures, and enhances hydrophobic residue exposure.
  • Revealed ribavirin enhances lysosomal activity and attenuates Aβ-induced ISR activation.
  • Efficacy was dependent on AMPK signaling, with selective action on stress responses.

Conclusions:

  • Ribavirin exhibits significant neuroprotective effects in AD models.
  • The drug acts by inhibiting Aβ aggregation and modulating cellular stress pathways.
  • Findings support repurposing ribavirin as a potential therapeutic agent for Alzheimer's disease.