Alzheimer disease (AD) is the most common cause of dementia among older people. One of the main features of AD is the presence in the brain of abnormal clumps of the protein fragment beta-amyloid, which are known as amyloid plaques. A team of researchers, led by Jens Pahnke, at the University of Rostock, Germany, has now identified a way to reduce the amount of beta-amyloid in the brains of mice with a disease that models AD, providing hope that a similar approach might be possible in patients.
One reason that beta-amyloid accumulates in the brain of an individual with AD is that it is cleared at a much reduced rate compared with that in the brain of an individual who is healthy. The mechanistic reasons for this reduced beta-amyloid clearance are not well known. But now, Pahnke and colleagues have determined that the transport protein ABCC1 has a key role in clearing beta-amyloid from the brain of mice. Of potential clinical interest, activation of ABCC1 using a drug approved by the FDA to relieve nausea and vomiting (thiethylperazine) markedly reduced the amount of beta-amyloid in the brains of mice with a condition that models AD. The authors therefore suggest that pharmacological activation of ABC transporters could perhaps impede the formation of amyloid plaques and thereby reduce the damage to the brain that results in dementia in individuals with AD.
TITLE: Cerebral amyloid-beta proteostasis is regulated by the membrane transport protein ABCC1 in mice
University of Rostock, Rostock, Germany.
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