Protein Interaction May be a Possible Cause of Alzheimer’s

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brainplaqueFor years, scientists have focused a majority of their Alzheimer’s research on two plaques found in the brain. Consisting of the proteins tau and amyloid-beta, these plaques have long been associated with the onset and progression of Alzheimer’s in patients. But a new neuroscience study focuses not on the proteins independently, but on how they interact with each other.

The neuroscience study, led by the Oregon National Primate Research Center, seems to show that the more interactions between the two proteins, the faster the progression of Alzheimer’s in both post-mortem human patients and animal subjects with the disease.

The research suggests that when these two proteins – most specifically in their toxic forms – interact during the moments of brain synapses, it causes immediate damage. And it’s this damage in synapses that leads to the cognitive dysfunctions and declines in Alzheimer’s patients.

The complex formation and interactions between the tau and amyloid-beta proteins blocks your brain from communicating properly with itself. Understanding how these interactions work, and how they lead to cognitive decline and the speeding up of the Alzheimer’s process, is the first step to a future cure. Learning to inhibit the binding of these proteins and plaques might very well be a viable cure for Alzheimer’s disease.

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