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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...
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...

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Related Experiment Video

Updated: May 7, 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

Anti-tau antibodies that block tau aggregate seeding in vitro markedly decrease pathology and improve cognition in

Kiran Yanamandra1,2,3, Najla Kfoury1,2,3, Hong Jiang1,2,3

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

Neuron
|October 1, 2013
PubMed
Summary

Monoclonal antibodies targeting extracellular tau aggregates reduced tau pathology, microglial activation, and improved cognition in a mouse model of tauopathies. This suggests immunotherapy blocking tau propagation is a promising treatment strategy.

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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

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In Vitro Assay for Studying the Aggregation of Tau Protein and Drug Screening
09:49

In Vitro Assay for Studying the Aggregation of Tau Protein and Drug Screening

Published on: November 20, 2018

Related Experiment Videos

Last Updated: May 7, 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

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
09:22

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

Published on: January 2, 2015

In Vitro Assay for Studying the Aggregation of Tau Protein and Drug Screening
09:49

In Vitro Assay for Studying the Aggregation of Tau Protein and Drug Screening

Published on: November 20, 2018

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Tau aggregation is a hallmark of neurodegenerative diseases like Alzheimer's.
  • Trans-cellular propagation of tau aggregates may drive disease pathogenesis.

Purpose of the Study:

  • To screen anti-tau monoclonal antibodies for blocking tau seeding activity.
  • To evaluate the therapeutic potential of effective antibodies in a mouse model.

Main Methods:

  • Screening anti-tau antibodies using a cell-based biosensor assay.
  • Infusing effective antibodies into P301S tau transgenic mice.
  • Assessing levels of hyperphosphorylated, aggregated, and insoluble tau.
  • Evaluating tau seeding activity, microglial activation, and cognitive function.

Main Results:

  • Three antibodies significantly reduced tau pathology, including hyperphosphorylation and aggregation.
  • Antibodies blocked the development of tau seeding activity in brain lysates.
  • Treatment led to reduced microglial activation and improved cognitive deficits in mice.

Conclusions:

  • Extracellular tau aggregates play a critical role in the development of tauopathies.
  • Immunotherapy targeting trans-cellular tau aggregate propagation is a viable treatment strategy.