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Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy
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Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy

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Fibrinogen and altered hemostasis in Alzheimer's disease

Marta Cortes-Canteli1, Daria Zamolodchikov, Hyung Jin Ahn

  • 1Laboratory of Neurobiology and Genetics, The Rockefeller University, New York, NY 10065, USA.

Journal of Alzheimer'S Disease : JAD
|August 8, 2012
PubMed

Insights

Alzheimer's disease involves amyloid-beta (Aβ) and fibrinogen. Their interaction forms resistant clots, worsening vascular issues and cognitive decline. Reducing fibrinogen improves outcomes in mouse models.

Area of Science:

  • Neuroscience
  • Pathology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) pathology includes amyloid-beta (Aβ) plaques, neurofibrillary tangles, and significant vascular dysfunction.
  • Vascular defects in AD encompass cerebrovascular dysfunction, reduced cerebral blood flow, and compromised blood-brain barrier (BBB) integrity.
  • The hemostatic system, particularly the clotting protein fibrinogen, is increasingly implicated in AD pathogenesis.

Purpose of the Study:

  • To review the link between amyloid-beta (Aβ) and vascular pathology in Alzheimer's disease.
  • To investigate the specific role of fibrinogen in Aβ deposition and associated neuroinflammation.
  • To explore the therapeutic potential of targeting Aβ-fibrinogen interactions.

Main Methods:

  • Review of existing literature on Aβ, fibrinogen, and vascular pathology in Alzheimer's disease.
  • Analysis of studies examining the interaction between Aβ and fibrinogen in AD models.
  • Evaluation of the effects of modulating fibrinogen levels on AD pathology and cognitive function in mouse models.

Main Results:

  • Amyloid-beta (Aβ) and fibrinogen interact, promoting Aβ fibrillization and forming degradation-resistant clots.
  • Elevated fibrinogen levels correlate with increased cerebral amyloid angiopathy, BBB permeability, and microglial activation.
  • Reducing fibrinogen levels in AD mouse models ameliorates vascular pathology and improves cognitive performance.
  • AD is characterized by a prothrombotic state, including increased clot formation and decreased fibrinolysis.

Conclusions:

  • Abnormal fibrinogen deposition, driven by Aβ interaction, contributes to AD progression, including neuroinflammation and neurodegeneration.
  • Targeting the interaction between fibrinogen and Aβ presents a promising therapeutic strategy for Alzheimer's disease.
  • Modulating the hemostatic system, specifically fibrinogen, may offer a novel approach to treating AD vascular pathology and cognitive decline.

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