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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'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...
Antibody Actions01:26

Antibody Actions

Antibodies, or immunoglobulins, are critical players in the immune system's arsenal against invading pathogens. Produced by B cells and plasma cells, their primary role is to detect and bind to specific antigens, molecules found on the surface of pathogens like bacteria or viruses. Beyond antigen recognition, antibodies perform several vital functions that contribute to immune defense.
Neutralization
Antibodies can bind to pathogens, preventing them from infecting host cells. This process...
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: May 16, 2026

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
07:18

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

Published on: November 9, 2018

Stealth attack: plaque-specific antibody allows for efficient Aβ removal without side effects.

Jee Hoon Roh1, David M Holtzman

  • 1Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.

Neuron
|December 11, 2012
PubMed
Summary
This summary is machine-generated.

A novel amyloid plaque-specific antibody effectively removes existing amyloid-beta (Aβ) aggregates in Alzheimer's disease models. This antibody shows promise as a safe and effective therapeutic for Alzheimer's disease, avoiding common side effects.

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Correlative Light and Electron Microscopy to Study Microglial Interactions with β-Amyloid Plaques
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Correlative Light and Electron Microscopy to Study Microglial Interactions with β-Amyloid Plaques

Published on: June 1, 2016

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

Related Experiment Videos

Last Updated: May 16, 2026

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
07:18

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

Published on: November 9, 2018

Correlative Light and Electron Microscopy to Study Microglial Interactions with β-Amyloid Plaques
10:52

Correlative Light and Electron Microscopy to Study Microglial Interactions with β-Amyloid Plaques

Published on: June 1, 2016

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Alzheimer's disease is characterized by amyloid plaques.
  • Current anti-amyloid beta (Aβ) antibody treatments face challenges with side effects and efficacy against existing plaques.

Discussion:

  • DeMattos et al. (2012) investigated a new antibody targeting amyloid plaques.
  • This plaque-specific antibody demonstrated the ability to clear pre-existing Aβ aggregates.

Key Insights:

  • The developed antibody successfully removed existing amyloid plaques.
  • Crucially, this clearance occurred without dose-limiting side effects.

Outlook:

  • This research suggests a potential new therapeutic strategy for Alzheimer's disease.
  • Further development could lead to safer and more effective Alzheimer's treatments.