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Inflaming the Brain

Hyung Jin Ahn1, Sarah K Baker2, Erin H Norris2

  • 1Department of Pharmacology, Physiology and Neurosciences, Rutgers-New Jersey Medical School, Newark, NJ 07103, USA; Brain Health Institute, Rutgers University, Piscataway, NJ 08854, USA.

Neuron
|March 22, 2019
PubMed

Insights

Blood-derived fibrinogen causes cognitive deficits and dendritic spine loss in Alzheimer's disease (AD) by activating microglial CD11b/CD18. This finding suggests fibrinogen is a key factor in AD pathogenesis.

Area of Science:

  • Neuroscience
  • Cerebrovascular Biology
  • Immunology

Background:

  • The precise role of cerebrovascular changes in Alzheimer's disease (AD) pathogenesis remains unclear.
  • Understanding the molecular mechanisms linking vascular factors to neurodegeneration is crucial for developing effective AD therapies.

Purpose of the Study:

  • To investigate the contribution of blood-derived fibrinogen to cognitive deficits in Alzheimer's disease.
  • To elucidate the cellular and molecular pathways through which fibrinogen impacts neuronal integrity and brain function.

Main Methods:

  • The study by Merlini et al. (2019) examined the effects of fibrinogen on neuronal structures and cognitive performance.
  • Investigated the role of microglial CD11b/CD18 in mediating fibrinogen-induced pathology.

Main Results:

  • Fibrinogen, a protein originating from the blood, was found to induce the elimination of dendritic spines, which are critical for synaptic function.
  • This fibrinogen-induced dendritic spine loss was associated with significant cognitive deficits.
  • The mechanism involves the activation of microglial CD11b/CD18 by fibrinogen.

Conclusions:

  • Blood-derived fibrinogen is implicated as a significant contributor to Alzheimer's disease pathogenesis.
  • Targeting fibrinogen or its interaction with microglial CD11b/CD18 may offer a novel therapeutic strategy for AD.

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