Alberto Pérez-Bouza

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Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder, characterized by a prominent loss of GABA-ergic medium-sized spiny neurons in the caudate putamen. There is evidence that impaired energy metabolism contributes to neuronal death in HD. Creatine is an endogenous substrate for creatine kinases and thereby supports cellular ATP(More)
Parkinson's disease is a disabling neurodegenerative disorder of unknown etiology characterized by a predominant and progressive loss of dopaminergic neurons in the substantia nigra. Recent findings suggest that impaired energy metabolism plays an important role in the pathogenesis of this disorder. The endogenously occurring guanidino compound creatine is(More)
Glial cell line-derived neurotrophic factor (GDNF) is a potent survival factor for ventral mesencephalic (VM) dopaminergic neurons. Subpopulations of dopaminergic and non-dopaminergic VM neurons express the calcium-binding proteins calbindin (CB) and calretinin (CR). Characterization of the actions of GDNF on distinct subpopulations of VM cells is of great(More)
Transplanted olfactory ensheathing cells (OECs) have previously been demonstrated to support axonal growth and myelination in the adult rat CNS. Here, the capacity of donor OECs to control the direction of axonal regeneration has been investigated following transplantation, as elongated columns, into the thalamus of adult rats. The OECs formed a 'glial(More)
Cell replacement therapy using mesencephalic precursor cells is an experimental approach for the treatment of Parkinson's disease (PD). A significant problem associated with this procedure is the poor survival of grafted neurons. Impaired energy metabolism is considered to contribute to neuronal cell death after transplantation. Creatine is a substrate for(More)
Up-regulation of the intermediate filament protein, nestin, is a sensitive indicator for the extent of astrocytic activation in regions of CNS close to the point of injury. However, it remains unclear whether activated astrocytes in distant, deafferented CNS territories are also capable of nestin re-expression. Here, we demonstrate that traumatic injury to(More)
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