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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...
Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
Alzheimer's Disease: Overview01:26

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...
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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Related Experiment Video

Updated: Jun 6, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
09:33

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

Published on: December 26, 2016

Immunotherapy for Alzheimer's disease.

D Morgan1

  • 1Alzheimer's Institute, University of South Florida, Tampa, FL 33613, USA. scientist.dave@gmail.com

Journal of Internal Medicine
|December 17, 2010
PubMed
Summary

Alzheimer's disease immunotherapy using anti-amyloid antibodies shows promise in clearing amyloid plaques and improving memory in mouse models and some human trials. However, risks like microhemorrhages and edema require further research for safer treatments.

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Amyloid precursor protein (APP) overproduction in transgenic mice leads to amyloid deposits.
  • Early studies showed vaccine and passive immunotherapy approaches could reduce amyloid and rescue memory deficits in mice.

Purpose of the Study:

  • To evaluate the efficacy and safety of anti-amyloid immunotherapies for Alzheimer's disease.
  • To investigate the potential of antibody-based treatments to clear amyloid plaques and improve cognitive function.

Main Methods:

  • Utilized transgenic mouse models overproducing amyloid precursor protein.
  • Conducted initial human clinical trials with vaccine and passive immunotherapy.
  • Employed passive immunotherapy with anti-amyloid antibodies in mouse models and human trials.

Related Experiment Videos

Last Updated: Jun 6, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
09:33

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

Published on: December 26, 2016

  • Monitored for cognitive benefits, amyloid clearance, and adverse events like microhemorrhages and edema.
  • Used positron emission tomography (PET) to assess amyloid burden reduction in trial participants.

    • Main Results:

    • Vaccine and passive immunotherapy reduced amyloid deposits and rescued memory deficits in mice.
    • Human trials showed some cognitive benefits and amyloid clearance, alongside autoimmune reactions.
    • Passive immunotherapy demonstrated effective amyloid clearance, even in older mice.
    • Observed microhemorrhages and increased vascular amyloid deposition as potential side effects.
    • Identified microhemorrhage and vasogenic edema in some patients, particularly those with apolipoprotein E4 genotype.
    • PET scans confirmed reduced amyloid burden in participants receiving anti-Aß antibody therapy over 18 months.

    Conclusions:

    • Anti-amyloid immunotherapies show significant potential for clearing amyloid plaques in Alzheimer's disease.
    • While demonstrating efficacy, these therapies carry risks of adverse events, including microhemorrhages and edema.
    • Further research is crucial to develop safer antibody variants that maintain amyloid clearance with reduced side effects.
    • Immunotherapy represents a key strategy for testing the amyloid hypothesis of Alzheimer's disease.