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RESEARCH PRODUCT
New Molecular Targets and Lifestyle Interventions to Delay Aging Sarcopenia
Alejandro LuciaHelios Pareja-galeanoFabian Sanchis-gomarSara MayeroCarme Perez-quilissubject
Gerontologymuscle atrophyAgingmedicine.medical_specialtySignaling pathwaysCognitive NeuroscienceFrailty syndromeEnvejecimientoSaludfrailtyCachexialcsh:RC321-571Internal medicinemedicineSenescence factorsPharmacological Targetslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrybusiness.industryPublic healthTestosterone (patch)Opinion Articlemedicine.diseaseMuscle atrophysignaling pathwayssenescence factorsSarcopeniaLean body massMolecular targetsMuscle atrophymedicine.symptombusinesspharmaceutical targetsNeurosciencedescription
The term sarcopenia was originally created to refer age-related loss of muscle mass with consequent loss of strength (Morley et al., 2001). There are now four international definitions of sarcopenia (Cruz-Jentoft et al., 2010; Muscaritoli et al., 2010; Morley et al., 2011). 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 <2 SDs 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 (Landi et al., 2012). 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 (Argiles et al., 2010). 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 (Cesari and Vellas, 2012; Landi et al., 2012). 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, such as those based on human growth hormone (hGH), IGF-1, testosterone, and stanozolol. 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 (Sanchis-Gomar et al., 2011), 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.
year | journal | country | edition | language |
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2014-07-01 | Frontiers in Aging Neuroscience |