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Scientific progress

08 - 02 - 2018

Senile dementia: the role of fibrinogen

Pericyte damage and fibrinogen accumulation may lead to a defect in the blood microcirculation of the brain and senile dementia.


Diffuse damage of the white matter of the brain, associated with capillary disease (small blood vessels) and a lack of blood circulation, are frequently described in senile dementia. But the origin of this damage remained unknown.


The brains of dead patients with Alzheimer's disease have half the normal amount of pericytes and three times more fibrinogen. Pericytes are the cells that surround the capillaries. They have a role of support, and metabolic and circulatory regulation. They are numerous in the capillaries of the brain. Fibrinogen is a protein that intervenes in coagulation.


To try to understand these phenomena, researchers created a line of transgenic mice deficient in pericytes. They then used different methods to see the consequences of this deficiency: MRI, tracers, behavioral tests and tissue analysis.




They discovered that a deficit of pericytes leads to:

  • - an accumulation of fibrinogen in the brain
  • - a reduction in blood microcirculation
  • - loss of myelin, axons and oligodendrocytes (myelin-producing cells)
  • Loss of motor functions comparable to those observed in senile dementia.


In vitro, fibrinogen causes the death of pericytes and oligodendrocytes. In vivo, the decrease in fibrinogen level almost completely repaires white matter.


These findings must be taken into account to better understand and treat white matter diseases and senile dementia, as well as Alzheimer's disease.