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Related Concept Videos

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

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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
09:22

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

Published on: January 2, 2015

Pre-aggregated Aβ1-42 peptide increases tau aggregation and hyperphosphorylation after short-term application.

Sabine Ott1, Andreas Wolfram Henkel, Maria Kerstin Henkel

  • 1Department of Psychiatry and Psychotherapy, University Hospital of Erlangen, Erlangen, Germany.

Molecular and Cellular Biochemistry
|November 30, 2010
PubMed
Summary

Pre-aggregated amyloid-beta (Aβ1-42) rapidly triggers tau protein hyperphosphorylation and aggregation in neuronal cells. This finding directly links the amyloid hypothesis to tau pathology in Alzheimer disease.

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Last Updated: Jun 6, 2026

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

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
04:41

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Alzheimer disease (AD) is characterized by amyloid plaques and neurofibrillary tangles.
  • The precise connection between amyloid-beta (Aβ) and tau pathology in AD remains unclear.

Purpose of the Study:

  • To investigate the effect of Aβ1-42 on tau hyperphosphorylation and aggregation.
  • To explore the functional and physiological link between Aβ and tau in Alzheimer disease.

Main Methods:

  • Overexpression of wildtype (2N4R) and mutant (P301L) tau constructs in SY5Y cells.
  • Incubation with pre-aggregated Aβ1-42.
  • Immunofluorescence microscopy to visualize tau aggregation.
  • Assessment of tau solubility.

Main Results:

  • Short incubation (90 min) with Aβ1-42 induced tau hyperphosphorylation and aggregation.
  • Aβ1-42 decreased tau solubility for both wildtype and mutant tau constructs.
  • Pathological changes in tau occurred rapidly in response to Aβ1-42.

Conclusions:

  • Pathological Aβ1-42 directly and rapidly induces tau hyperphosphorylation and aggregation.
  • This study provides a direct link between the amyloid hypothesis and tau pathology in Alzheimer disease.
  • Findings suggest Aβ's role in initiating tau-related neurodegeneration.