The protein fragment beta-amyloid is a key suspect in Alzheimer's disease. This fragment tends to accumulate into long chains called fibrils, which in turn lead to the larger clumps (or plaques) that are a hallmark of Alzheimer's. However, current research suggests that beta-amyloid is most toxic during the earliest stages of accumulation, when it forms small clusters called oligomers. These oligomers have been shown to damage the brain's synapses, or the tiny channels through which brain cells communicate with one another. Such synaptic damage leads to dementia-related cognitive decline. However, the exact mechanisms by which oligomers exert their toxicity are unknown. This lack of knowledge is due, in part, to the nature of studying oligomer activity in Alzheimer's-like mice. These engineered animals tend to possess both oligomers and fibrils at the same time—making it difficult to sort out the toxic properties of oligomers from those of fibrils.
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- Alzheimer's Association