{"id":17113,"date":"2014-12-10T16:20:47","date_gmt":"2014-12-10T15:20:47","guid":{"rendered":"http:\/\/ibecbarcelona.eu\/?page_id=17113"},"modified":"2026-01-16T14:47:29","modified_gmt":"2026-01-16T13:47:29","slug":"molecular-and-cellular-neurobiotechnology","status":"publish","type":"page","link":"https:\/\/ibecbarcelona.eu\/es\/neurobiotechnology","title":{"rendered":"Molecular and Cellular Neurobiotechnology"},"content":{"rendered":"
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About<\/h2>\n
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Our research interests are focused on three main aspects of developmental neurobiology and neurodegeneration:<\/span><\/span> development of new lab on chip devices for neurobiological research<\/span>, new strategies to avoid \u03b1-synuclein and tau transport in neurons<\/i> and new approaches to enhance axon regeneration after lesion.<\/h4>\n\n\n\n

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Development of new lab on chip devices for neurobiological research <\/span><\/span><\/strong><\/p>\n\n\n\n

One of our focus is to mimic the developing and neurodegenerating nervous system in lab on chip devices. We believe that combining several different stimuli in the chip resembles a more realistic environment that nerve cells will encounter in the living animal in normal and disease conditions. These experiments using la bon chip models in turn will make future studies on the role of neuronal cells in development and regeneration more accurate and complete. Thus, we developed a new device able to reproduce the formation of the neuromuscular junction (NMJ) in lab on chip devices. In addition, a device designed to analyse axon lesions of cortical neurons was also developed. <\/p>\n\n\n\n

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We developed a new device able to reproduce the formation of the neuromuscular junction (NMJ) in lab on chip devices.<\/p>\n<\/blockquote>\n\n\n\n

Current experiments of our group in collaboration with groups of IBEC, CIBER-BBN, and other labs aimed at developing new lab on chip devices to mimics and modulate particular neurobiological processes. For example: i) on chip lab platform to monitor drug delivery modulating neuronal activity (see figure); ii) cortico-spinal chips to develop axon regenerative studies of new drug formulation (in collaboration with Imperial College; London); iii) devices tmigrating neurons (in collaboration with i3A, Zaragoza) and, iv) in silico 3D modeling for neurodegenerative diseases (Alzheimer and Parkinson chip).<\/p>\n\n\n\n

Last experiments are focused to reproduce a lab on chip devices to analyse and to reproduce ALS models (in collaboration(Alzheimer and Parkinson chip). Last experiments are focused to reproduce a lab on chip devices to analyse and to reproduce ALS models (in collaboration with Biodonostia Hospital) (Figure 2).<\/p>\n\n\n\n

New strategies to avoid \u03b1-synuclein and tau transport in neurons <\/strong><\/p>\n\n\n\n

\u03b1<\/span>-Synuclein is a key player in the pathogenesis of <\/span>synucleinopathies<\/span>, including <\/span>Parkinson\u2019s disease, dementia with Lewy bodies, and multiple system atrophy. Transmission of synthetic <\/span>\u03b1<\/span>-synuclein aggregates has been demonstrated in several cellular and animal models. Several groups have reported that insoluble <\/span>\u03b1<\/span>-synuclein shows <\/span>\u201c<\/span>prion-like<\/span>\u201d<\/span> propagation in wild-type mice. However, the basis of the spreading process remains poorly understood although cell to cell <\/span>transport via exocytosis has been proposed. <\/span>We described in 2018 that <\/span>PrP<\/span>C<\/span>\u202fis <\/span>a new receptor for <\/span>\u03b1<\/span>-synuclein<\/span> involved in their spreading and <\/span>propagatio<\/span>n. Our new objectives aimed to block this interaction to reduce the neuropathological transport of <\/span>\u03b1<\/span>-synuclein<\/span>. Similar experiments are also developed in the case of tau, one of the hallmarks of Alzheimer\u00b4s disease, since tau also binds to <\/span>PrP<\/span>C<\/span> during its inter-<\/span>neuronal propagation.<\/span> <\/p>\n\n\n\n

New approaches to enhance axon regeneration after lesion <\/strong><\/p>\n\n\n\n

 Following axonal lesions in the adult CNS, damaged axons degenerate, while surviving fibres are unable to regenerate, and have a limited capacity to sprout and to re-establish lost connections. Experimental evidence suggests that providing a permissive extracellular environment containing cellular or biomaterial bridges is not enough to increase axon regrow to obtain functional regeneration, supporting the importance of clarifying the complex transcriptional response below these signalling pathways. As an alternative, activating or recapitulating the developmental program of the lesioned neuron to sprout and regenerate may represent a complementary therapeutic approach and may sometimes directly counteract the inhibitory signalling. Optogenetics is currently the state-of-the-art method for activity-based nervous system research, allowing more specific cellular stimulations by light in a less invasive techniques compared to classical electrical stimulation, but leading to a more tailored physiological response3. In our laboratory, we started to analyse whether optical stimulation of lesioned neurons is able to enhance axonal growth or sprouting. These experiments were performed on lesioned cortical neurons in vitro<\/span><\/i> and <\/span>in vivo<\/span><\/i>.  <\/span><\/p>\n\n\n\n

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Caption<\/figcaption><\/figure>\n\n\n\n
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Example of fluorescence microscopy picture showing one example\nof cultured hippocampal neurons extending their neuritis inside a microchannel in a microfluidic lab on a chip device after 15 days in culture. The axon of the neurons is labeled in green and the dendrites in red<\/figcaption><\/figure>\n\n\n\n
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Primary neuronal culture from mouse embryo after 7 days in vitro. Neurons are labelled in green and astrocytes in red<\/figcaption><\/figure>\n\n\n\n
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Primary neuronal culture. Neurons (green) and astrocytes (red) derived from a E16.5 eGFP transgenic mouse embryo after 15 days in vitro<\/figcaption><\/figure>\n\n\n\n
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Calcium waves in cultured cortical neurons growing on compartimentalized lab on chip devices.<\/figcaption><\/figure>\n\n\n\n
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Figure 2) Example of a monolayer of ChR2-expressing C2C12 myotubes on compartmentalized lab on chip devices showing the traction vector forces during cell contraction after 470 nm light stimulation<\/figcaption><\/figure>\n<\/figure>\n\n\n\n<\/div>

Staff<\/h2>\n
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