There is plenty of evidence for progressive dysfunction in neurotransmission related to GABA to be important in forms of cognitive decline, particularly relating to memory. A number of approaches to treat this loss have been considered, with the one noted here the most recent of the type. Exactly why GABA-related dysfunction occurs in the brain is a matter for debate; as for so much of aging, there is no well-mapped line of cause and consequence leading from the fundamental damage that causes aging to the observed changes in cell behavior the aging brain. There are two approaches to dealing with this ignorance. The first is to repair the well-known forms of damage, and see what happens - the SENS rejuvenation biotechnology methodology. The second, far more popular, approach is to try to compensate for the late stage, downstream dysfunction in some way, without addressing the causes.
This second strategy, the far worse strategy, describes near all of the development of medicine for age-related disease over the past century, and its dominance in the research community is why little progress has been made. There is nothing harder than trying to keep a damaged machine running without repairing the damage. Nonetheless, as capacities in biotechnology grow, these attempts do become incrementally better. It is still absolutely the wrong approach to the challenge, but people continue to be lured back in by the steady improvement in outcomes. Of course, given that most prior outcomes are marginal at best, it doesn't take much for new initiatives to look better in comparison.
New therapeutic molecules show promise in reversing the memory loss linked to depression and aging. What's unique and promising about these findings, in the face of many failures in drug development for mental illness, is that the compounds are highly targeted to activate the impaired brain receptors that are causing memory loss. Researchers first identified the specific impairments to brain cell receptors in the GABA neurotransmitter system. Then they showed that these impairments likely caused mood and memory symptoms in depression and in aging.
The new small molecules were invented to bind to and activate this receptor target. The idea was that they would exert a therapeutic effect by "fixing" the impairment, resulting in an improvement in symptoms. The molecules are chemical tweaks of benzodiazepines, a class of anti-anxiety and sedative medications that also activate the GABA system, but are not highly targeted.
A single dose of these new molecules was administered in preclinical models of stress-induced memory loss. Thirty minutes later, memory performance returned to normal levels, an experiment that was reproduced more than 15 times. In another experiment involving preclinical models of aging, memory declines were rapidly reversed and performance increased to 80 per cent after administration, essentially reaching levels seen in youth or earlier stages of adulthood. This improvement lasted over two months with daily treatment.