Alzheimer’s treatment: Mouse study investigates blood replacement

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The aggregation of the beta-amyloid protein into insoluble deposits in the brain is a hallmark of Alzheimer’s disease. A recent study shows that replacing blood in a mouse model of Alzheimer’s disease with blood from healthy wild-type mice could slow down the formation of beta-amyloid deposits.

This blood exchange treatment also improved spatial memory in the Alzheimer’s disease mouse model. The study could facilitate the development of novel treatments for Alzheimer’s disease that target proteins or other factors in the blood. A new study published in Molecular PsychiatryTrusted Source demonstrated that replacing the blood of an Alzheimer’s disease (AD) mouse model with the blood of a wild-type mouse reduced the levels of AD brain markers and improved spatial memory in the mouse model.

Although the mechanisms underlying these findings remain unclear, the results suggest that manipulating certain components in the blood could help treat AD. Targeting components in the blood for the treatment of AD can help bypass the challenges associated with developing drugs that can cross the blood-brain barrier. AD is the most common form of dementiaTrusted Source, accounting for 60-80%Trusted Source of all dementia cases. More than 6 million individuals in the United States currently have AD and projections indicate that this number is may reach 13 million by 2050. Thus, there is an urgent need for effective treatments for this condition.

A central characteristic of AD is the abnormal accumulation of the beta-amyloid protein into deposits, known as plaques, in the brain. Single units, or monomers, of the beta-amyloid protein tend to aggregate together to form short chains called oligomers. These soluble oligomers aggregate to form fibrils, which later form insoluble plaques. Experts consider these beta-amyloid aggregates to be responsible for the damage to brain cells in AD. Beta-amyloidmonomers are produced in the brain and also in other organs. Beta-amyloid monomers and oligomers can cross the blood-brain barrier, passing from the brain to the blood and from the blood to the brain. The beta-amyloid protein is broken down in peripheral organsTrusted Source, including the kidneys and the liver, which explains its presence in blood.

Moreover, researchTrusted Source suggests that there is a close association between beta-amyloid levels in the brain and the bloodstream. In a studyTrusted Source conducted using a genetically engineered — or transgenic — AD mouse model, receiving blood from older, transgenic mice with beta-amyloid deposits accelerated the formation of beta-amyloid deposits in younger transgenic animals.

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