It is well known in the stroke field for example that the magnitude of recovery after focal lesion is greater in children than in older adults. However, we can find in the literature CHIR99021 FDA Arguments both for and against the capacity of the older brain to adapt to pathological conditions. We can also find arguments to positive or negative effects of drug plasticity changes in aged people. From basic science Brain

plasticity Inhibitors,research,lifescience,medical in old animals Arguments can be found in the literature for compromised brain remodeling and plasticity associated with age.62-67 Arguments are summarized in a remarkable review by Hermann and Chopp.21 Aged rats respond to plasticity-promoting therapies, but age might have an effect on some of the processes targeted by neurorestorative interventions. Improved neurological recovery associated with

preservation of pyramidal tract axons ipsilateral to the stroke and enhanced pyramidal tract sprouting contralateral to the stroke was identified in 25-month-old or 12-month-old Inhibitors,research,lifescience,medical rats with ischemia treated with neutralizing anti-NogoA antibodies, pharmacological compounds, or bone-marrow-derived Inhibitors,research,lifescience,medical stromal cells. Although neurological recovery was successful, dendritic and synaptic plasticity of hippocampal CA3 and CA1 pyramidal and dentate gyrus granule cells was not influenced by anti-NogoA antibodies in old rats. The expression of plasticity-related proteins in neurons differs between young and old animals. An effect of age was not only seen for neuronal sprouting, but also for neurogenesis and angiogenesis. The numbers of proliferating neural precursor Inhibitors,research,lifescience,medical cells in the subventricular zone and subgranular layer were lower in the brain tissue of 15-month-old rats than in that of 3-month-old

rats, both under normal physiological and ischemic conditions. Although the de novo generation of neurons in the ischemic striatum was very similar in both groups, neurogenesis was decreased in the dentate gyrus of 15-month-old rats when exposed to focal cerebral ischemia. Inhibitors,research,lifescience,medical Reduced neurogenesis in old animals could be related to lower expression of VEGFR2 on the surface of neural precursor cells. Although evidence is limited to a rather small number of studies, the preserved neurological recovery in old animals argues against specific age limits for neurorestorative Cilengitide treatments. Despite this evidence, the effects of age need to be controlled in clinical proof-of-concept studies.62-67 Comorbidities, vascular risk factors, and brain plasticity Vascular risk factors are often associated with stroke and so also with aging.68-71 They are part of the question and we can find also arguments in basic science for compromised brain remodeling and plasticity associated with vascular risk factors. Experimental studies poorly mimic comorbidities, because experiments are done mainly in animals that are otherwise healthy.