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A Neuroprotector's Dilemma


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Posted 02 October 2014 - 10:34 AM


Here is a recent article from the SENS Research Foundation, a review of recent work in the broader research community relating to the development of neuroprotective drugs and proteins, ways to help brain cells resist the damage of aging:

The aging brain is characterized by the accumulation of a variety of proteinaceous aggregates, high levels of which constitute the distinctive neuropathological hallmarks and (in the consensus view) the underlying drivers of the neurodegenerative diseases of aging. Removal of these aggregates from the brain is therefore a central damage-repair strategy to prevent and arrest the course of "normal" cognitive aging and its diagnostically-specified extreme manifestations. Happily, this subfield of rejuvenation research has been advanced further toward medical availability than any other, with new strategically-positioned trials of Aβ immunotherapies and of a first-in-class α-synuclein vaccine.

Another pillar of comprehensive neurorejuvenation is cell therapy for the aging brain. However, cell therapy to preserve and restore the neuronal circuitry underlying higher-order cognitive functions in the aging brain is a much more formidable undertaking. Unlike with other major organs such as the heart or kidneys - or even the repair of dopaminergic brain circuitry as exhibited prominently in Parkinson's disease - wholesale replacement of brain functional units is undesirable, due to the structural basis of memory and identity. Thus, a more sophisticated and gradualist approach is required, in which existing circuits are rebuilt and reinforced by ongoing integration of transplanted neurons and precursors, in such a way as to maintaining their existing architecture.

Neuroprotective agents offer a potential stopgap, to hold the therapeutic window open in the period between the availability of aggregate-clearing immunotherapies and the development of neuronal replacement techniques. From first principles, one might anticipate that in a scenario in which therapeutic clearance of some aggregate had been achieved, the most effective neuroprotective agents would be those that target mechanisms of neurodegeneration that are not directly downstream of these aggregates. However, it is also likely that in the earliest iterations of these therapies, their specificity, range of action, therapeutic index, pharmacokinetics, or other properties may limit the scope and magnitude of clearance that can be achieved in a given round of application, so that even agents that allow vulnerable neurons to survive the downstream effects of these aggregates may yet deliver some neuroprotective benefit.

Link: http://www.sens.org/...gent-janus-face


View the full article at FightAging




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