Percorrer por autor "Castelo-Branco, Miguel"
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- Brain activity during lower-limb movement with manual facilitation: an fMRI studyPublication . Almeida, Patrícia Maria Duarte de; Vieira, Ana Isabel Correia Matos de Ferreira; Canário, Nádia Isabel Silva; Castelo-Branco, Miguel; Caldas, Alexandre Lemos de CastroBrain activity knowledge of healthy subjects is an important reference in the context of motor control and reeducation. While the normal brain behavior for upper-limb motor control has been widely explored, the same is not true for lower-limb control. Also the effects that different stimuli can evoke on movement and respective brain activity are important in the context of motor potentialization and reeducation. For a better understanding of these processes, a functional magnetic resonance imaging (fMRI) was used to collect data of 10 healthy subjects performing lower-limb multijoint functional movement under three stimuli: verbal stimulus, manual facilitation, and verbal + manual facilitation. Results showed that, with verbal stimulus, both lower limbs elicit bilateral cortical brain activation; with manual facilitation, only the left lower limb (LLL) elicits bilateral activation while the right lower limb (RLL) elicits contralateral activation; verbal + manual facilitation elicits bilateral activation for the LLL and contralateral activation for the RLL. Manual facilitation also elicits subcortical activation in white matter, the thalamus, pons, and cerebellum. Deactivations were also found for lower-limb movement. Manual facilitation is stimulus capable of generating brain activity in healthy subjects. Stimuli need to be specific for bilateral activation and regarding which brain areas we aim to activate.
- Intestinal mucosal alterations parallel central demyelination and remyelination: insights into the gut-brain axis in the cuprizone model of multiple sclerosisPublication . Ferreira, Carolina; Carvalho, Filipa; Vieira, Pedro; Alves, André; Palavra, Filipe; Almeida, Jani; Alves, Vera; Coscueta, Ezequiel; Pereira, Patrícia Dias; Pintado, Manuela; Sá, Helena; Castelo-Branco, Miguel; Reis, Flávio; Viana, SofiaBackground: The gut-brain axis has been increasingly recognized as a critical factor in Multiple Sclerosis (MS) pathophysiology. While its role in demyelination is well documented, gut-brain axis involvement during remyelination remains largely unexplored. Methods: Using the cuprizone (CPZ) model, which induces reversible demyelination and spontaneous remyelination upon toxin withdrawal, we investigated gut and brain changes during both disease stages in C57BL/6 mice. Animals were administered 0.2% cuprizone for 5 weeks to induce demyelination, followed by a 2-week recovery phase. Intestinal changes were evaluated through 1) gut microbiota profiling and metabolite production (short-chain fatty acids (SCFAs), indoxyl sulfate), 2) structural and barrier integrity via histology, mucus staining, and tight junction markers (ZO-1, occludin, claudin-5), 3) mucosal immunity through M1/M2 macrophage profiling and Th17/Treg ratios, and 4) expression of inflammatory and oxidative stress markers. Differences in brain demyelination/remyelination, gliosis and related molecular changes were determined using immunohistochemistry and real-time polymerase chain reaction (RT-PCR). Results: The demyelination peak was characterized by reduced abundance of SCFA-producing genus Akkermansia and Dubosiella, increased intestinal permeability at the level of the mucus layer and tight junction networks, and shifts in mucosal immunity toward a pro-inflammatory state characterized by M1 macrophages and Th17 cell expansion together with elevated levels of inflammatory cytokines (IL-17, IL-1?) and changes in oxidative stress-related enzymes (iNOS, HO-1, SOD1/2), all of which were partially reversed during the remyelination phase. Centrally, cuprizone-induced demyelination/remyelination and gliosis showed region-specific patterns. Neuroinflammation peaked during demyelination (TNF-?, IL-1?, IL-6, IL-17) and only partially resolved, suggesting that a balanced inflammatory response may aid remyelination. Conclusion: Our findings reveal that cuprizone-induced intestinal dysfunctions temporally parallel central nervous system (CNS) lesion dynamics, disclosing temporal coordination of both compartments and highlighting gut-brain axis impact on both disease stages.