Sarcopenia is the name given to age-related loss of muscle mass and and strength, although by the time it is processed through the regulatory system into a formal, final disease definition, it will be restricted to referring to only severe levels of loss. Average loss of muscle mass and strength will be called normal, just a part of aging, and therefore something that shouldn't be treated - and indeed, that it is forbidden to treat, as in regulatory systems like that of the FDA in the US, everything that is not explicitly permitted is illegal. This is a major systemic problem with the present system of medical regulation, one that has to be changed, and soon. It is no wonder that we see only slow progress in research and fundraising when treating degenerative aging is largely forbidden, especially any focus on causes and prevention rather than patching over late stage consequences after the fact.
Here is an open access review of a range of approaches in mainstream research aimed at slowing the onset and progression of sarcopenia, most of which haven't made it as far as drug development yet. As for so many of these topics it overwhelmingly focuses on alteration of metabolic processes rather than repair of root causes: slowing the progression of damage only, not reversing it.
The term sarcopenia was originally created to refer age-related loss of muscle mass with consequent loss of strength. There are now four international definitions of sarcopenia. In essence they all agree, requiring a measure of walking capability [either low gait speed or a limited endurance (distance) in a 6-min walk], together with an appendicular lean mass of [less than 2 standard deviations below] of a sex and ethnically corrected normal level for individuals 20-30 years old. Sarcopenia is a prevalent health problem among the elderly. On average, 5-13% and 11-50% of people aged 60-70 years and ≥80 years, respectively suffer sarcopenia with higher prevalences (68%) been reported in nursing home residents ≥70 years.
Sarcopenia needs to be differentiated from cachexia, which is a combination of both muscle and fat loss and is usually attributable to an excess of catabolic cytokines associated with a disease process. Sarcopenia is a prime component of the frailty syndrome, and both sarcopenia and frailty are associated with increased disability, falls, hospitalization, nursing home admission, and mortality.
Medical efforts to develop treatments aiming at preventing aging sarcopenia as well as acute muscle atrophy and frailty in critical patients are considered a step forward in public health. Several hormonal therapies have been proposed for this purpose. However, the secondary effects associated with these therapies make it necessary to find novel non-toxic and non-hormonal therapies. In this way, elderly or bedridden patients may improve muscle function and decrease the degree of dependence associated with these populations. New drugs such as allopurinol or losartan, all of them approved by the Food and Drugs Administration (FDA) and actually prescribed for the treatment of other diseases, could be useful in preventing loss of muscle mass in the described susceptible populations yet new pharmacological targets are needed.
As an essential step for the prevention of aging-related diseases, and specifically, sarcopenia, more basic research is needed on the main cellular hallmarks of muscle senescence. There is a plethora of potential molecular signals that are candidates to be targeted in future treatment strategies aiming at combating sarcopenia, a devastating effect of aging that is often overlooked.