The high level strategy for the development of rejuvenation therapies should be to target and revert known changes, at least in those cases where we can put forward good evidence for the change to occur due to the normal operation of metabolism. This is on the basis that amyloid is not observed in any significant amount in young tissues. Not all cellular reactions to the damage and change of aging are beneficial: there are plenty of examples of antagonistic pleiotropy to pick from, in which cellular behavior that helps in the context of a youthful environment is far less benign in the context of aged tissues.Įven before attaining a complete understanding of the biochemistry of any particular amyloid, a task that the Alzheimer's research community has demonstrated to be very challenging, we should be guided towards a strategy of removal. Clearing out the amyloid should nonetheless be beneficial, either by removing a source of those errant and damaging molecules, or by damping the reaction of cells to its presence, something that may also be a problem. This environment and its interactions with cells has proven to be exceedingly complex, like most areas of interest to modern medicine. In those cases where the biochemistry of an amyloid is well explored, as for amyloid-β, it appears that it is not the amyloid per se that is the problem, but the surrounding halo of related compounds. Others remain more obscure, and it is even possible that some do not contribute meaningfully to aging over a normal human life span. Some amyloids are very well associated with specific age-related diseases, as is the case for amyloid-β and Alzheimer's disease, and as is becoming the case for transthyretin amyloid and cardiovascular disease. There are a score or so of different types of amyloid, each corresponding to a particular protein that can become misfolded in a way that makes it precipitate and clump into solid aggregates between cells. Amyloids are one of the distinguishing features of old tissues, absent in the tissues of younger individuals. The open access paper for today takes a look at amyloid formation and some of the cellular processes that try to hold it back, processes that become increasingly disarrayed with advancing age.
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