We have found that loss of communication between brain cells and blood vessels leads to build up of the b-amyloid protein in a mouse model of Alzheimer’s disease. This helps us understand how Alzheimer’s disease develops and may provide new avenues to develop treatments for Alzheimer’s disease.
Alzheimer’s disease (AD) affects more than 35 million people worldwide. AD causes problems with thinking, remembering and reasoning. Current treatments for AD do not stop or reverse the disease, so more information is needed to develop ways to prevent and treat the disease.
b-amyloid (Ab) is a toxic protein that builds up in the AD brain. Ab is normally removed from the brain along blood vessels that receive signals from brain cells. In AD, the brain cells that release the chemical acetylcholine die and this communication is lost. In this study, we examined if loss of communication between cholinergic brain cells and blood vessels of the brain contributes to the build-up of Ab in AD.
To replicate the death of brain cells observed in AD, mice carrying a human AD gene were given a drug to kill cholinergic brain cells. 45 days later, their brains were examined for levels of Ab.
We found that there was more Ab in the blood vessels of mice who received the drug compared to mice whose cholinergic brain cells were still intact.
Our findings suggest that communication between brain cell and blood vessels is indeed important for the efficient removal of Ab from the brain. Maintaining this communication would help prevent the build-up of Ab and possibly delay the onset or severity of AD. Therefore, it may be beneficial to start treatment with drugs that increase acetylcholine in people with memory problems early on.
This work supports an important role for blood vessel health in the development of Alzheimer’s disease. Our hope is to develop new preventative and therapeutic strategies focused on vascular health to treat Alzheimer’s disease.Dr Cheryl Hawkes
Senior Lecturer in Health SciencesVisit Cheryl's profile