Navegando por Assunto "Spike protein"

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    Analysis of the Sars-cov-2 virus spike protein in 2D and 3D neuronal models of Alzheimer's disease associated with photobiomodulation treatment
    (2026-04-17) Soares, Cristina Pacheco; Sant'Anna, Luciana Barros; Ito, Cristiane Yumi Koga; Andrade, Erick José Nogueira de; São José dos Campos
    Alzheimer's disease (AD) is the leading cause of dementia worldwide, characterized by a complex pathophysiological scenario involving neuroinflammation and intense oxidative stress. At the same time, the COVID-19 pandemic has raised concerns about the neurodegenerative effects of the SARS-CoV-2 spike protein. Considering that oxidative stress is a central mechanism shared by both AD and the sequelae of COVID-19, this work used hydrogen peroxide (H2O2) as an experimental model of oxidative insult. The objective was to investigate how the spike protein enhances cellular damage and to evaluate the neuroprotective potential of photobiomodulation (PBM) with red LED (660 nm) in these contexts. For this, SHSY5Y cells differentiated into two-dimensional (2D) and three-dimensional (3D) neuronal models were used. The cells were exposed to recombinant spike protein (0.5 µg/mL) and H2O2 (200 µM), either individually or in combination, to simulate an aggravated toxicity environment. Cell viability and metabolism were monitored using the Alamar Blue assay and flow cytometry (Live/Dead). Confocal microscopy analyses allowed for the evaluation of nuclear (Hoechst), mitochondrial (MitoTracker), cytoskeletal (rhodamine-phalloidin), and focal adhesion (FAK) integrity. Additionally, a model of neuronal spheroids (3D) was standardized to mimic a more physiologically relevant microenvironment. The results in the 2D model indicated that the spike protein and H2O2 significantly reduced cell viability, with intensified cytotoxic effects upon co-exposure. In contrast, the 3D model exhibited an adaptive response, maintaining viability and increasing metabolic activity, suggesting that tissue architecture modulates neuronal resilience. PBM (3 J/cm²) proved effective in preserving mitochondrial and structural morphology, reducing apoptosis both under basal conditions and oxidative stress, especially in the 3D model. Together, the data reinforce that the Spike protein exerts distinct effects depending on the cellular model and highlight PBM as a promising therapeutic strategy to mitigate oxidative stress and preserve neuronal function in neurodegenerative pathologies and viral sequelae.