The major focus of research into the biochemical causes and manifestations of Alzheimer dementia (AD) has largely been characterized by a rather pinpoint and straightforward course. Relegated to the foundations of disease genesis within the cerebrospinal fluid and in cerebral neurons, discoveries in this facet of AD research have yielded much in the way of prior (development of cholinesterase inhibitors to treat AD symptoms) and future treatments (tau and beta amyloid protein modifiers, etc). The common theme with respect to those discoveries depended heavily on neurons already found to be diseased with the abnormal proteins and the like.

With the recent news of new research techniques involving the role of abnormal proteins in healthy cells, researchers hope to detect the onset of cellular changes responsible for initiating the AD cascade as it is happening, thus opening the potential for new mechanisms of disease and treatment. Although it is exciting to document the genesis of abnormal neuronal signals that may herald the early changes seen in asymptomatic AD patients, it is even more exciting to begin to search for the potential to turn off this mechanism completely. | LINK

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