In a recent study, researchers have discovered a new cause of the cognitive decline in Alzheimer’s disease.
The finding may help develop new diagnosis and treatment tools for people with Alzheimer’s.
The research was conducted by scientists at the Gladstone Institutes.
Previous research has shown that patients with Alzheimer’s disease have abnormalities in the blood vessels in the brain.
Some of these changes may also lead to age-related cognitive decline in people without dementia.
However, how such vascular pathologies contribute to cognitive dysfunction has been unclear.
In the study, the team found that a blood-clotting protein called fibrinogen is responsible for a series of molecular and cellular changes.
These changes could destroy connections between neurons in the brain and cause cognitive decline.
The researchers used state-of-the-art imaging technology to study both mouse brains and human brains with Alzheimer’s disease.
They also generated the first 3D volume images that showed blood-brain barrier leaks occur in Alzheimer’s disease.
They found that the protein fibrinogen could activate the brain’s immune cells and triggers them to destroy important connections between neurons.
This occurred after the protein leaked from the blood into the brain.
Previous research has shown that elimination of the connections can lead to memory loss, a common feature in Alzheimer’s disease and other dementias.
The team suggests that the findings provide new information about the cause and possible cure of cognitive decline in Alzheimer’s disease and other neurological diseases.
They suggest that vascular changes in the brain may need to be targeted with separate therapies to prevent cognitive decline in dementia.
The team recently has developed an antibody that blocks the interaction between fibrinogen and a molecule on the brain’s immune cells.
They hope future work will help develop a new method to treat cognitive decline.
The leader of the study is Senior Investigator Katerina Akassoglou, Ph.D.
The study is published in the journal Neuron.
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