000			na a22 4500
999			_c724 _d724
003			PC724
005			20210625062754.0
008			130622s2013 xxx||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_aBautista, José M. _91902 _eInstituto de Investigación i+12
100			_aDíez, Amalia _91901 _eInstituto de Investigación i+12
100			_aLinares Gómez, María _91898 _eInstituto de Investigación i+12
100			_aMarín García, Patricia _92240 _eInstituto de Investigación i+12
100			_aPuyet, Antonio _91900 _eInstituto de Investigación i+12
245	0	0	_aBrain-derived neurotrophic factor and the course of experimental cerebral malaria _h[artículo]
260			_bBrain Research, _c2013
300			_a1490:210-24.
500			_aFormato Vancouver: Linares M, Marín-García P, Pérez-Benavente S, Sánchez-Nogueiro J, Puyet A, Bautista JM et al. Brain-derived neurotrophic factor and the course of experimental cerebral malaria. Brain Res. 2013 Jan 15;1490:210-24.
501			_aPMID: 23123703
504			_aContiene 64 referencias
520			_aThe role of neurotrophic factors on the integrity of the central nervous system (CNS) during cerebral malaria (CM) infection remains obscure, but the long-standing neurocognitive sequelae often observed in rescued children can be attributed in part to the modulation of neuronal survival and synaptic plasticity. To discriminate the contribution of key responses in the time-sequence of the pathogenic events that trigger the development of neurocognitive malaria syndrome we defined four stages (I-IV) of the neurological progression of CM in C57BL/6 mice infected with Plasmodium berghei ANKA. Upregulation of ICAM-1, VCAM-1, e-selectin and p-selectin expression was detected in all cerebral regions before parasitized red blood cells (pRBC) accumulation. As the severity of symptoms increased, BDNF mRNA progressively diminished in several brain regions, earliest in the thalamus-hypothalamus, cerebellum, brainstem and cortex, and correlated with a four-stage disease sequence. Immunohistochemical confocal microscopy revealed changes in the BDNF distribution pattern, suggesting altered axonal transport. During CM progression, molecular markers of neurological infection and inflammation in the parasite and the host, respectively, were accompanied by a switch in the brain constitutive proteasome to the immunoproteasome, which could impede normal protein turnover. In parallel with BDNF downregulation, NCAM expression also diminished with increased CM severity. Together, these data suggest that changes in BDNF availability could be involved in the pathogenesis of CM.
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/7/pc724.pdf _ySolicitar documento
942			_n0 _2ddc _cART