Cartas enviadas por José Manuel Barrenechea a Justo Garate entre 1981 y 1982

4 cartas (manuscritas) ; entre 210x260mm y 150x200mm

Tarjeta postal enviada por José M. Barrenetxea a Justo Garate en 1971

1 tarjeta postal (manuscrita) ; 150x100mmm

Cartas enviadas por José Mª Barriola a Justo Garate entre 1958 y 1965

2 cartas (manuscritas) ; entre 210x210mm y 210x160mm

Cartas enviadas por José Belbey a Justo Garate entre 1954 y 1956

2 cartas (manuscritas) ; 135x220mm

Cartas enviadas por José María Bengoa a Justo Garate entre 1940 y 1945

10 cartas (mecanografiadas); entre 210x255mm y 210x310mm. [La carta fechada el 10-11-1942 esta incompleta, falta la primera hoja]

Cartas enviadas por José María Bengoa a Justo Garate entre 1947 y 1961

11 cartas (mecanografiadas y manuscritas); entre 170x225mm y 215x275mm

Cartas enviadas por José María Bengoa a Justo Garate entre 1962 y 1992

8 cartas (mecanografiadas y manuscritas); entre 150x210mm y 215x275mm .- 1 Felicitación de Navidad (manuscrita y sin fecha) ; 110mmx160mm

Carta enviada por José Berruezo a Justo Garate en 1973

1 carta (mecanografiada) ; 215x300mm

Differential Neuroprotective Effects of 5 '-Deoxy-5 '-Methylthioadenosine

Background: 5'-deoxy-5'-methylthioadenosine (MTA) is an endogenous compound produced through the metabolism of polyamines. The therapeutic potential of MTA has been assayed mainly in liver diseases and, more recently, in animal models of multiple sclerosis. The aim of this study was to determine the neuroprotective effect of this molecule in vitro and to assess whether MTA can cross the blood brain barrier (BBB) in order to also analyze its potential neuroprotective efficacy in vivo. Methods: Neuroprotection was assessed in vitro using models of excitotoxicity in primary neurons, mixed astrocyte-neuron and primary oligodendrocyte cultures. The capacity of MTA to cross the BBB was measured in an artificial membrane assay and using an in vitro cell model. Finally, in vivo tests were performed in models of hypoxic brain damage, Parkinson's disease and epilepsy. Results: MTA displays a wide array of neuroprotective activities against different insults in vitro. While the data from the two complementary approaches adopted indicate that MTA is likely to cross the BBB, the in vivo data showed that MTA may provide therapeutic benefits in specific circumstances. Whereas MTA reduced the neuronal cell death in pilocarpine-induced status epilepticus and the size of the lesion in global but not focal ischemic brain damage, it was ineffective in preserving dopaminergic neurons of the substantia nigra in the 1-methyl-4-phenyl-1,2,3,6-tetrahydro-pyridine (MPTP)-mice model. However, in this model of Parkinson's disease the combined administration of MTA and an A(2A) adenosine receptor antagonist did produce significant neuroprotection in this brain region. Conclusion: MTA may potentially offer therapeutic neuroprotection.