Llibres / Capítols de llibre (Patologia i Terapèutica Experimental)

URI permanent per a aquesta col·leccióhttps://diposit.ub.edu/handle/2445/178728

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    Multilingual Naming
    (Springer, 2021-07-08) Fernandez Coello, Alejandro; Gil Robles, Santiago; Carreiras, Manuel
    Bi/multilingualism refers to the ability to use two or more languages in everyday life. Increasing interest has been paid to unveil the neural basis of bilingual language processing; however, the brain representation of language in bilinguals is still a matter of debate. Currently, there is a weak level of evidence supporting that the best probable way to avoid a selective language deficit is to perform multilingual intraoperative tests. The key point is to individualize and tailor—depending on daily needs—the neuropsychological protocol, from testing only the native language up to testing all the languages the patient speaks. Furthermore, the bilingual brain is capable of handling both languages without apparent difficulty or interference. This cognitive ability, which includes language switching, has also been studied and mapped. Results suggest a functional cortico-subcortical network that takes advantage both from language-specific areas and from nonspecific cognitive control regions, working together to maintain effective communication. Therefore, electrical stimulation mapping arises not only as a technique to maintain the quality of life of bilingual patients but also as a useful tool in neurocognitive research.
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    Epigenetic Modulation of Adenosine A2A Receptor: A Putative Therapeutical Tool for the Treatment of Parkinson’s Disease
    (IntechOpen, 2011-11-02) Barrachina Castillo, Marta; Martín, Mairena; Ciruela Alférez, Francisco; Ferrer, Isidro (Ferrer Abizanda)
    Adenosine is a nucleoside distributed throughout the entire organism as an intermediary metabolite. At the extracellular level, adenosine plays multiple physiologic roles, interacting with specific receptors: A1, A2A, A2B and A3 (Fredholm et al., 2001). While the A1Rs and A3Rs are coupled in an inhibitory way to adenylate cyclase through the Gi/o protein, the A2Rs are coupled in a stimulatory way to this enzymatic activity through Gs protein (Ralevic & Burnstock, 1998). Adenosine levels are increased after ischemia, hypoxia, excitotoxicity, inflammation and cerebral lesions. In these situations, it is considered that high adenosine levels play a neuroprotective role (Ribeiro et al., 2002). Interestingly, adenosine regulates the release of glutamate, the main excitatory neurotransmitter of the nervous system (Sebastiao & Ribeiro, 1996). A1Rs are widely expressed in the brain and have been shown to modulate neuronal excitability by decreasing pre-synaptic release of various neurotransmitters (Fredholm & Dunwiddie, 1988). The most dramatic inhibitory actions are on the glutamatergic system (Masino et al., 2002). In the central nervous system (CNS), A1Rs are associated with neuroprotective processes (Angulo et al., 2003; Dunwiddie and Masino, 2001). Moreover, they are upregulated in human neurodegenerative diseases with abnormal protein aggregates and it is related to compensatory mechanisms (Albasanz et al., 2007, 2008; Angulo et al., 2003; Perez-Buira et al., 2007; Rodríguez et al., 2006). Regarding A2ARs, these receptors are concentrated in the striatum, modulating dopaminergic activity, but they are also present in the hippocampus and cerebral cortex, modulating the glutamate release in the brain. Adenosine activity through A2 receptors (A2ARs) can eventually give rise to neurotoxicity, neuronal damage and cellular death (de Mendoça et al., 2000). In fact, A2ARs activity is associated with the outcome of cerebral injury as well as the development of Abeta- induced synaptotoxicity (Canas et al., 2009; Cunha, 2005; Stone et al., 2009).
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    Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research
    (IntechOpen, 2011-09-06) Albasanz, José Luis; Castillo, Carlos Alberto; Barrachina Castillo, Marta; Ferrer, Isidro (Ferrer Abizanda); Martín, Mairena
    Senescence-accelerated mouse (SAM) lines serve as models of aging and age-associated diseases. The SAMP8 strain has a shortened life span and early-onset manifestations of senescence with characteristic pathological features observed in elderly humans, including deficits in learning and memory. In brains of SAMP8 mice, the processing of amyloid precursor protein (APP) is altered, resulting in excess production and accumulation of amyloid-􀇃 peptide (A􀇃), tau is hyper-phosphorylated, and oxidative stress is increased. These phenotypic abnormalities are quite reminiscent of the findings in human brains with Alzheimer’s disease (AD). Mechanistically, metabolic pathways that are responsible for the generation of reactive oxygen species (ROS) are increased, while antioxidant systems are reduced in activity in the cerebral cortex of aged SAMP8 mice. Besides these structural and metabolic alterations, brains of aged SAMP8 mice exhibit neurochemical abnormalities such as altered signaling through G protein-coupled receptors for 5-hydroxytryptamine, acetylcholine, adenosine, dopamine, melatonin, glutamate and GABA, ion channel receptors, and nuclear hormone receptors (e.g. for all-trans-retinoic acid, cortisol or estradiol). Consequences include alterations in the levels of neurotransmitters, receptor numbers, receptor binding affinity, and second messengers. Of note is that in AD, G proteincoupled receptors and/or their corresponding signaling pathways are often impaired. Together, the observations in aged SAMP8 mouse brains provide convincing evidence that this model serves as an excellent research tool for studying AD pathogenesis and strategies for treatment. Additionally, many of the pathological and neurochemical abnormalities in SAMP8 mice are linked to altered expression of genes that are integrally related to processes such as neuroprotection, signal transduction, protein folding/degradation, intracellular transport and immune response. Several studies have already utilized pharmacological or dietary measures to restore cognitive function and enhance neuroprotection in aged SAMP8 mice, suggesting that these approaches may have applications in the treatment of AD. This review compiles available data concerning the signaling pathways that are altered in SAMP8 mice, and compares the effects to known abnormalities in AD brains.