New Research Challenges Current Beliefs on How Nerve Cells Die in Alzheimer’s Disease

New Research Challenges Current Beliefs on How Nerve Cells Die in Alzheimer’s Disease
The buildup of beta-amyloid plaques in the brain is not sufficient on its own to cause the death of neurons in Alzheimer’s disease, suggests a new study that challenges current views on how the disease progresses. Researchers have widely believed that beta-amyloid drives nerve cell death in Alzheimer's, but these results open up the possibility that other mechanisms could contribute to disease progression. The study, “The Impact of APP on Alzheimer-like Pathogenesis and Gene Expression in Down Syndrome iPSC-Derived Neurons,” was published in the journal Stem Cell Reports. Accumulation of beta-amyloid plaques in the brain, one of the hallmarks of Alzheimer's, occurs when a protein called the amyloid precursor protein (APP) is broken down, and its fragments, called beta-amyloid, clump together. University of Queensland researchers used induced pluripotent stem cells (iPSCs) — adult cells capable of generating almost any cell in the body — from people with Down syndrome to better understand the role APP and amyloid plaques play in the death of nerve cells. Those with Down syndrome, a condition in which a person is born with extra genetic material from chromosome 21, have a significantly increased risk of developing early-onset Alzheimer disease (before age 65). According to the Down Syndrome Society<
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    While interesting results, it has been well established for 20 years that the actual AD causative agents are the soluble small amyloid-beta oligomers and not plaque. Something that W. Klein from Northwestern University clearly showed in 1998. In fact, plaque seems to be a protection mechanism that sequesters the toxic oligomers. Also, new data shows that many elderly with high levels of plaque are cognitively normal, despite the plaque accumulation. Indeed, new procedures are allowing to measure those oligomers, which apparently form quite quickly after certain damaging events and in the absence of plaque.

  2. Arthur Bollon says:

    Not only need APP precursor but also need abnormal processing of the APP protein for the pathology. Simply increasing APP doesn’t address the abnormal processing.

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