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<p>The formation of amyloid Aβ<sub>42</sub>-fibrils is linked to the pathology of cognitive dysfunction in Alzheimer’s patients. There is a dire need for developing therapeutics to reverse Aβ<sub>42</sub> fibrillation and to stop or slow down the disease progression. Here, we report rationally designed sialic acid functionalized porphyrin cored first and second-generation dendrimers, synthesized using “click chemistry.” The glycoporphyrin dendrimer shows a promising ability to degrade Aβ<sub>42</sub> fibrils to lower-order soluble oligomers upon irradiation. The gradual fragmentation of the β-sheet-rich Aβ<sub>42</sub> fibrils to the unstructured forms by photoactivation of the dendrimers is evident from high-resolution imaging, particle size analysis, and peptide secondary structure distribution. Further, the glycodendrimers are non-toxic even when irradiated and can rescue the neuroblastoma cells from Aβ<sub>42</sub> fibril-mediated cytotoxicity. We propose that the photoirradiated dendrimers degrade the Aβ<sub>42</sub> fibrils by rupturing the H-bonds by the singlet oxygen species (ROS) generated from the excited porphyrin core.</p><p></p>

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Photolytic disruption of Alzheimer’s amyloid Aβ42-fibrils by sialic-acid decorated glycodendrimers

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月26日

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  • Rituparna Das,
  • Swarnendu Roy,
  • Rahul Das,
  • Balaram Mukhopadhyay

摘要

The formation of amyloid Aβ42-fibrils is linked to the pathology of cognitive dysfunction in Alzheimer’s patients. There is a dire need for developing therapeutics to reverse Aβ42 fibrillation and to stop or slow down the disease progression. Here, we report rationally designed sialic acid functionalized porphyrin cored first and second-generation dendrimers, synthesized using “click chemistry.” The glycoporphyrin dendrimer shows a promising ability to degrade Aβ42 fibrils to lower-order soluble oligomers upon irradiation. The gradual fragmentation of the β-sheet-rich Aβ42 fibrils to the unstructured forms by photoactivation of the dendrimers is evident from high-resolution imaging, particle size analysis, and peptide secondary structure distribution. Further, the glycodendrimers are non-toxic even when irradiated and can rescue the neuroblastoma cells from Aβ42 fibril-mediated cytotoxicity. We propose that the photoirradiated dendrimers degrade the Aβ42 fibrils by rupturing the H-bonds by the singlet oxygen species (ROS) generated from the excited porphyrin core.