In the view of the SENS Research Foundation, some of the present large-scale scientific work to reverse the accumulation of beta-amyloid protein (Aβ) associated with Alzheimer's disease (AD) is a form of rejuvenation biotechnology. Amyloids of all sorts are on the list of aging-associated changes that should be repaired in order to revert old tissue to the same state it had when young. The hope here is that many of the technologies developed by the Alzheimer's research community can be repurposed to address other types of unwanted compounds that accumulate between cells:
A key target for rejuvenation biotechnologies to prevent and arrest the course of AD is the removal of aggregated beta-amyloid protein (Aβ) from the brain. Amongst the constellation of factors playing some role in the pathogenesis of AD, there is now a strong case for the thesis that Aβ aggregates are at the root of its aetiology. Moreover, Aβ has also been implicated in the cognitive deficits clinically present in other age-related neurological diseases. For example, brain Aβ deposits and abnormally low levels of Aβ42 in the cerebrospinal fluid (CSF) discriminate people suffering from Parkinson's disease dementia and dementia with Lewy bodies from those suffering from Parkinson's disease but whose cognition remains intact. And even amongst people whose cognition is still within the normal range, the presence of Aβ plaque as detected [on] Positron Emission Tomography (PET) is associated with cognitive deficits and increased rate and extent of gray mattter atrophy.
The need for disease-modifying therapies in AD, and the strength of the case for Aβ as a target, have recently driven substantial regulatory reform and innovations in clinical trial design to accommodate more effective testing of Aβ immunotherapies targeting the removal of Aβ from the brain. The first fruits of these changes are the initiation of a series of large, late-stage clinical trials of Aβ vaccines in the early clinical or even preclinical phases of the disease. These reforms have wider and even more hopeful implications, because they open up the path for faster and more meaningful clinical trials of other rejuvenation biotechnologies as they emerge.
The move by scientists and regulators to begin administering Aβ immunotherapy not only early in clinical dementia, but during the preclinical phase of the disease, is an extremely important development. The new regulatory posture responds to the recognition that the volunteers in these trials are not merely "at high risk of Alzheimer's," but are fated to dementia (and to the many other diseases and disabilities of aging) unless rescued by rejuvenation biotechnology - a fate, it must be emphasized, shared by us all, as part of the degenerative aging process.