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<p>Alzheimer’s disease (AD) is a major cause of dementia and remains a significant global health challenge, with no curative treatments currently available. The COVID-19 pandemic has raised concerns regarding neurological complications associated with SARS-CoV-2, particularly the role of the Spike protein in neurotoxicity. This study investigated the neurotoxic effects of recombinant Spike protein in a two-dimensional (2D) in vitro model of oxidative-induced neuronal injury, as well as the potential protective role of photobiomodulation (PBM, 3&#xa0;J/cm²) using a red LED (660&#xa0;nm). Differentiated SH-SY5Y cells were exposed to Spike protein (0.5&#xa0;µg/mL) and H₂O₂ (200 µM), individually or in combination, with or without PBM. Cell viability was assessed using the Alamar Blue assay, while immunofluorescence analysis was performed to evaluate nuclear morphology, mitochondrial integrity, cytoskeletal organization, and focal adhesion dynamics. Flow cytometry (Annexin V/PI and CellROX) was used to quantify apoptosis, cell death, and intracellular reactive oxygen species (ROS). Results demonstrated that the Spike protein induced mitochondrial fragmentation, cytoskeletal disorganization, and increased oxidative stress, leading to enhanced apoptotic susceptibility. These effects were exacerbated under oxidative conditions, indicating a synergistic interaction. PBM attenuated these alterations by reducing ROS levels, apoptosis, and structural damage, while preserving cellular integrity. Overall, these findings indicate that the Spike protein acts as a modulator of redox imbalance, contributing to neuronal dysfunction in an in vitro oxidative stress model. PBM emerges as a promising non-pharmacological strategy capable of mitigating these effects through modulation of mitochondrial function and cellular redox homeostasis.</p>

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From neurotoxicity to neuroprotection: photobiomodulation against the effects of the SARS-CoV-2 spike protein in a 2D neurodegenerative model using differentiated SH-SY5Y cells

  • 期刊论文

  • 发表日期：

    2026年5月20日

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  • Erick José Nogueira de Andrade,
  • Geisa Rodrigues Salles,
  • Luiza de Andrade Giraldi,
  • Milena Yuki Rosental Sudo,
  • Lucas de Paula Ramos,
  • Cristina Pacheco-Soares

摘要

Alzheimer’s disease (AD) is a major cause of dementia and remains a significant global health challenge, with no curative treatments currently available. The COVID-19 pandemic has raised concerns regarding neurological complications associated with SARS-CoV-2, particularly the role of the Spike protein in neurotoxicity. This study investigated the neurotoxic effects of recombinant Spike protein in a two-dimensional (2D) in vitro model of oxidative-induced neuronal injury, as well as the potential protective role of photobiomodulation (PBM, 3 J/cm²) using a red LED (660 nm). Differentiated SH-SY5Y cells were exposed to Spike protein (0.5 µg/mL) and H₂O₂ (200 µM), individually or in combination, with or without PBM. Cell viability was assessed using the Alamar Blue assay, while immunofluorescence analysis was performed to evaluate nuclear morphology, mitochondrial integrity, cytoskeletal organization, and focal adhesion dynamics. Flow cytometry (Annexin V/PI and CellROX) was used to quantify apoptosis, cell death, and intracellular reactive oxygen species (ROS). Results demonstrated that the Spike protein induced mitochondrial fragmentation, cytoskeletal disorganization, and increased oxidative stress, leading to enhanced apoptotic susceptibility. These effects were exacerbated under oxidative conditions, indicating a synergistic interaction. PBM attenuated these alterations by reducing ROS levels, apoptosis, and structural damage, while preserving cellular integrity. Overall, these findings indicate that the Spike protein acts as a modulator of redox imbalance, contributing to neuronal dysfunction in an in vitro oxidative stress model. PBM emerges as a promising non-pharmacological strategy capable of mitigating these effects through modulation of mitochondrial function and cellular redox homeostasis.