Alzheimer’s disease (AD), the leading cause of dementia, is a disease of the brain – or is it? A study by University of British Columbia and Chinese scientists published in Molecular Psychiatry* in 2017, suggests future drug therapies may be able to reverse or delay AD without acting directly on the brain, which is a difficult area to target.
The scientists in this particular research study demonstrated the brian:body nexus through a technique called parabiosis, which involves surgically attaching two animals together so they share the same blood supply for several months. In this case, the Canadian and Chinese researchers attached normal mice, which don’t naturally develop AD, to AD mice that carry a mutant human gene that produces high levels of a protein called Ab. The Ab protein accumulates in the brain and forms clumps, or plaques, which decrease communication within the brain and trigger brain cell death. Mice with the Ab protein display human-like AD symptoms as they grow older.
The researchers in this study found that the normal mice that were joined to the mice with high levels of the Ab protein also contracted Alzheimer’s disease. The researchers believe that the Ab traveled through the blood from the Ab mice to the brains of their normal partners, where it accumulated and caused damage to their brain. Not only did the normal mice develop plaques, but they also developed other signs of AD including brain cell degeneration, inflammation and micro bleeds. Their ability for normal learning and memory was also impaired.
Until this experiment, it was unclear if Ab from outside the brain could contribute to AD. This study not only reveals that blood-derived Ab can enter the brain and trigger AD like pathology, it also indicates that in the aging brain, it might allow more Ab to infiltrate the brain and accelerate brain deterioration. Thus, the researchers envision a future drug that binds to and clears Ab before it reaches the brain.
* Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies. Bu XL, Xiang Y, et al.
Molecular Psychiatry. 2017 Oct 31. doi: 10.1038/mp.2017.204
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