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Related Concept Videos

Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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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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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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Amyloid Fibrils03:03

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Amyloid Fibrils03:03

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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Immune Response Against Viral Pathogens01:29

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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Small interfering RNAs, or siRNAs, are short regulatory RNA molecules that can silence genes post-transcriptionally, as well as the transcriptional level in some cases. siRNAs are important for protecting cells against viral infections and silencing transposable genetic elements.
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Related Experiment Video

Updated: Nov 14, 2025

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
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Viral Involvement in Alzheimer's Disease.

Ahmad Sait1,2,3, Cristian Angeli1,2, Andrew J Doig4

  • 1Division of Evolution and Genomic Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester M13 9PL, United Kingdom.

ACS Chemical Neuroscience
|March 9, 2021
PubMed
Summary

Human herpes simplex virus-1 (HSV-1) may play a role in Alzheimer's disease (AD) pathogenesis. Valacyclovir, an HSV-1 treatment, showed cognitive improvements in AD patients, suggesting further research into this link.

Keywords:
Alzheimer’s diseaseapolipoprotein Eblood−brain barrierherpes simplex virusvalacyclovirβ-amyloid

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Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Pathology

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid plaques and neurofibrillary tangles.
  • AD prevalence is rising globally, with no approved therapeutics despite numerous failed clinical trials.
  • The causative agent of AD remains unknown, prompting investigation into potential contributing factors like pathogens.

Purpose of the Study:

  • To explore the potential role of human herpes simplex virus-1 (HSV-1) in the pathogenesis of Alzheimer's disease.
  • To review evidence linking HSV-1 presence in the brain to AD pathology.
  • To discuss the implications of valacyclovir's cognitive effects in AD patients.

Main Methods:

  • Review of existing literature on HSV-1, AD, and potential therapeutic interventions.
  • Analysis of factors contributing to HSV-1 pathogenicity in the context of neurodegeneration.
  • Examination of clinical study findings related to valacyclovir and cognitive function in AD patients.

Main Results:

  • Human herpes simplex virus-1 (HSV-1) has been detected in the brains of both AD patients and controls.
  • HSV-1 possesses mechanisms that could contribute to AD pathology, including latency, tau phosphorylation, and Aβ accumulation.
  • Clinical studies indicate that valacyclovir, an antiviral medication, may improve cognitive function in AD patients.

Conclusions:

  • HSV-1 is a potential contributor to Alzheimer's disease pathogenesis.
  • Further research is warranted to investigate the causal relationship between HSV-1 and AD.
  • Antiviral therapies targeting HSV-1 represent a potential avenue for AD treatment.