Paradoxically, treatment with bone-marrow-derived stromal cells did not improve neurological recovery in rats with diabetes, but increased mortality, blood-brain barrier leakage, and brain hemorrhage. In histochemical studies, neo intima formation and arteriole narrowing were exacerbated by bone-marrow-derived stromal cells in rats with diabetes, as was macrophage accumulation in blood vessels. These abnormalities were attributed to increased angiogenin expression in the brain and brain-supplying arteries of rats with diabetes. Investigators suggest that treatment with bone-marrow-derived Inhibitors,research,lifescience,medical stromal cells should

not be considered in patients with diabetes. Three-quarters of stroke patients have arterial hypertension, and about half of patients have hypercholesterolemia. In spontaneously hypertensive rats, subtle abnormalities in the expression of neurotrophic

factors and their receptors have been described Inhibitors,research,lifescience,medical in the dentate gyrus. Whether these findings are true for prolonged arterial hypertension, which causes cerebral microangiopathy in human beings, remains Inhibitors,research,lifescience,medical to be shown. Hypercholesterolemia reduces angiogenesis and promotes blood-brain barrier permeability. These vascular changes are driven by many factors. In rats with cerebral ischemia, vitamin B3 administration, which elevates high-density lipoprotein and thereby reduces serum cholesterol, increased angiogenesis, and improved Inhibitors,research,lifescience,medical neurological recovery. Moreover, despite limited evidence, recent studies suggest that impaired angiogenesis

in patients with hypercholesterolemia parallels disturbances in synaptic plasticity. Lipid-lowering drugs, especially statins, are widely prescribed for stroke patients Inhibitors,research,lifescience,medical as secondary stroke prevention. Statins also have neurorestorative properties. From clinical data Clinical data mainly do not confirm basic science evidence of the reduced capacity of brain to reorganize after a focal lesion or during a chronic neurodegenerative disease in aging. Even if we have clinical selleck arguments to say that post-stroke clinical recovery is reduced in old people, clinicians have all seen remarkable recovery in patients over 85. Moreover, it has been recently demonstrated that IV thrombolysis could be beneficial in people over 80 Levetiracetam as recently shown in IST3 trial.72 Thus, even if the biological counterpart of brain plasticity is reduced in old age, clinical recovery exists in old people. The stroke model has shown this. This preserved capacity is much more difficult to demonstrate in chronic degenerative disease where recovery does not exist. However, we know that people with memory disturbances in early AD are able to recruit alternative brain networks to perform a memory task. This has been shown with fMRI by Pariente et al.73 Interventional studies also provide evidence for preserved brain capacity to reorganize in the elderly.