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Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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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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Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
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Autoreactive-Aβ antibodies promote APP β-secretase processing.

Juan Deng1, Huayan Hou, Brian Giunta

  • 1Rashid Laboratory for Developmental Neurobiology, Department of Psychiatry and Neurosciences, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.

Journal of Neurochemistry
|December 23, 2011
PubMed
Summary

Alzheimer's disease patients produce autoantibodies that may unexpectedly increase amyloid-beta generation by activating beta-secretase. This finding is crucial for understanding Alzheimer's disease etiology and developing future immunotherapies.

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Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain
10:08

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain

Published on: August 28, 2012

Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is linked to amyloid-beta (Aβ) accumulation.
  • Naturally occurring autoantibodies against Aβ exist in AD patients, but their functional roles are poorly understood.
  • Existing research often focuses on antibody concentration or binding affinity, neglecting functional impacts.

Purpose of the Study:

  • To investigate the functional properties of naturally occurring autoantibodies against Aβ in Alzheimer's disease patients.
  • To determine if Aβ-targeting autoantibodies influence amyloid precursor protein (APP) processing.
  • To explore the potential role of these autoantibodies in the etiology of sporadic AD.

Main Methods:

  • Isolation and characterization of Aβ-reactive autoantibodies from AD patients and healthy controls.
  • Assaying autoantibody effects on β-secretase activity in cultured cells.
  • Utilizing monoclonal antibodies targeting specific Aβ regions (e.g., Aβ(1-17)) to study APP processing.
  • Dose-dependent analysis of antibody impact on amyloidogenic APP processing.

Main Results:

  • Naturally occurring Aβ-reactive autoantibodies from AD patients, but not controls, enhanced β-secretase activity in cultured cells.
  • Monoclonal antibodies targeting the N-terminal region of Aβ, particularly Aβ(1-17), dose-dependently promoted amyloidogenic APP processing.
  • Antibody binding to the N-terminus of Aβ correlated with increased Aβ generation via β-secretase activation.

Conclusions:

  • Certain autoantibodies targeting Aβ in AD patients can promote Aβ generation by activating β-secretase.
  • This autoantibody-driven Aβ production may contribute to the etiology of sporadic Alzheimer's disease.
  • Future anti-Aβ immunotherapies must consider potential detrimental effects of N-terminal targeting antibodies on APP processing and Aβ generation.