Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Correction: APOE4-Expressing Astrocytes Exhibit Parkinson's Disease-Related Pathology.

Molecular neurobiology·2026
Same author

Human Microglial Molecular Alterations in Aging and Alzheimer's Disease.

Cells·2026
Same author

Nasal administration of Protollin enhances monocyte phagocytosis and decreases CD8<sup>+</sup> T cell cytotoxicity in subjects with early Alzheimer's disease: a Phase 1 clinical trial.

npj aging·2026
Same author

Beneficial effect of lactate in neurodegenerative diseases: Association with downregulation of C-X-C motif chemokine receptor 4 signaling.

Neural regeneration research·2026
Same author

Drug Development.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2025
Same author

Curiouser and curiouser: Meningeal lymphoid structures in the aging brain.

Proceedings of the National Academy of Sciences of the United States of America·2025

Related Experiment Video

Updated: Jun 13, 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.

Beka Solomon1, Dan Frenkel

  • 1Department of Molecular Microbiology & Biotechnology, George S. Wise Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Tel Aviv, Israel. beka@post.tau.ac.il

Neuropharmacology
|April 15, 2010
PubMed
Summary

Alzheimer's disease (AD) research focuses on amyloid-beta (Abeta) peptide, a key factor in AD pathogenesis. Immunotherapy targeting Abeta shows promise for clearing brain plaques and developing new treatments.

Related Experiment Videos

Last Updated: Jun 13, 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

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • The amyloid cascade hypothesis posits that amyloid-beta (Abeta) peptide accumulation drives Alzheimer's disease (AD) pathogenesis.
  • Abeta aggregation and oligomerization are critical early events in AD, leading to neurodegeneration and memory impairment.

Purpose of the Study:

  • To explore the role of the immune system in AD pathogenesis.
  • To investigate the potential of immunotherapy targeting Abeta for AD treatment.

Main Methods:

  • Utilizing transgenic mouse models that overproduce human Abeta and exhibit AD-like pathology.
  • Evaluating immunological approaches to stimulate the clearance of amyloid plaques in the brain.

Main Results:

  • Evidence suggests immune system involvement in AD pathogenesis, including partial tolerance to Abeta.
  • Immunization strategies have shown potential for clearing brain amyloid plaques in animal models.

Conclusions:

  • The central role of Abeta in AD is reinforced, validating it as a therapeutic target.
  • Ongoing clinical trials are refining immunotherapeutic strategies for AD, aiming for efficacy without adverse effects.