2024-03-28T17:30:44Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/608812021-12-27T16:43:46Zcom_10261_54com_10261_1col_10261_307
Circulating insulin-like growth factor I mediates the protective effects of physical exercise against brain insults of different etiology and anatomy
Carro, Eva
Trejo, José L.
Busiguina, S.
Torres Alemán, Ignacio
Physical exercise ameliorates age-related neuronal loss and is currently recommended as a therapeutical aid in several neurodegenerative diseases. However, evidence is still lacking to firmly establish whether exercise constitutes a practical neuroprotective strategy. We now show that exercise provides a remarkable protection against brain insults of different etiology and anatomy. Laboratory rodents were submitted to treadmill running (1 km/d) either before or after neurotoxin insult of the hippocampus (domoic acid) or the brainstem (3-acetylpyridine) or along progression of inherited neurodegeneration affecting the cerebellum (Purkinje cell degeneration). In all cases, animals show recovery of behavioral performance compared with sedentary ones,i.e., intact spatial memory in hippocampal-injured mice, and normal or near to normal motor coordination in brainstem- and cerebellum-damaged animals. Furthermore, exercise blocked neuronal impairment or loss in all types of injuries. Because circulating insulin-like growth factor I (IGF-I), a potent neurotrophic hormone, mediates many of the effects of exercise on the brain, we determined whether neuroprotection by exercise is mediated by IGF-I. Indeed, subcutaneous administration of a blocking anti-IGF-I antibody to exercising animals to inhibit exercise-induced brain uptake of IGF-I abrogates the protective effects of exercise in all types of lesions; antibodyt-reated animals showed sedentary-like brain damage. These results indicate that exercise prevents and protects from brain damage through increased uptake of circulating IGF-I by the brain. The practice of physical exercise is thus strongly recommended as a preventive measure against neuronal demise. These findings also support the use of IGF-I as a therapeutical aid in brain diseases coursing with either acute or progressive neuronal death.
2012-11-22T12:52:40Z
2012-11-22T12:52:40Z
2001
2012-11-22T12:52:40Z
artículo
Journal of Neuroscience 21: 5678- 5684 (2001)
0270-6474
http://hdl.handle.net/10261/60881
10.1523/JNEUROSCI.21-15-05678.2001
11466439
eng
closedAccess
Society for Neuroscience