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<p>Aging-induced neurodegeneration is characterized by cognitive impairment, elevated oxidative stress, neuroinflammation, synaptic loss, and neuronal death. Atraric acid (AA), a phenolic compound obtained from lichens, is reported to have potent anti-inflammatory and antioxidant effects in various disease models. However, aging-induced cognitive impairment and dementia are still not elucidated. To fill this gap, we investigated AA (20&#xa0;mg/kg/day, intraperitoneally (i.p.) for 4&#xa0;weeks) against <span>d</span>-galactose (<span>d</span>-gal) (120&#xa0;mg/kg/day, i.p. for 8&#xa0;weeks)-induced brain senescence and memory dysfunction in mice. Behavioral tests, including NOR, MWM, and Y-maze, were conducted to assess cognitive function, followed by biochemical and immunofluorescence analyses. AA restored the BDNF/TrkB/Akt signaling axis disrupted by <span>d</span>-gal administration. Furthermore, immunoblotting for Nrf-2 and HO-1 revealed elevated expression in the mouse cortex and hippocampus. AA also enhanced antioxidant enzymes, including glutathione (GSH), glutathione S-transferase (GST), catalase (CAT), and superoxide dismutase (SOD), while reducing lipid peroxidation (LPO), thereby supporting its antioxidant role. Moreover, <span>d</span>-gal enhanced NF-kB-mediated neuroinflammation, apoptotic markers including caspase-3 and PARP-1, and suppressed synaptic proteins (SNAP-23 and PSD-95). Interestingly, these expression aberrations were reversed upon AA administration. Histological analyses using Nissl and Fluoro-Jade B staining further supported neuronal protection in the cortex and hippocampus. Collectively, these findings suggest that AA exerts neuroprotective effects against <span>d</span>-gal-induced aging and cognitive decline by reducing oxidative stress, neuroinflammation, neuronal apoptosis, and enhancing synaptic plasticity through BDNF/TrkB/Akt/CREB signaling.</p> Graphical abstract <p></p>

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Atraric acid enhances neuronal survival and cognition against d-galactose-induced neurodegeneration via BDNF/TrkB/AKT signaling

  • 期刊论文

  • 发表日期：

    2026年7月7日

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  • Talha Nasir,
  • Kyonghwan Choe,
  • Hyun Young Park,
  • Min Hwa Kang,
  • Tae Ju Park,
  • Myeong Ok Kim

摘要

Aging-induced neurodegeneration is characterized by cognitive impairment, elevated oxidative stress, neuroinflammation, synaptic loss, and neuronal death. Atraric acid (AA), a phenolic compound obtained from lichens, is reported to have potent anti-inflammatory and antioxidant effects in various disease models. However, aging-induced cognitive impairment and dementia are still not elucidated. To fill this gap, we investigated AA (20 mg/kg/day, intraperitoneally (i.p.) for 4 weeks) against d-galactose (d-gal) (120 mg/kg/day, i.p. for 8 weeks)-induced brain senescence and memory dysfunction in mice. Behavioral tests, including NOR, MWM, and Y-maze, were conducted to assess cognitive function, followed by biochemical and immunofluorescence analyses. AA restored the BDNF/TrkB/Akt signaling axis disrupted by d-gal administration. Furthermore, immunoblotting for Nrf-2 and HO-1 revealed elevated expression in the mouse cortex and hippocampus. AA also enhanced antioxidant enzymes, including glutathione (GSH), glutathione S-transferase (GST), catalase (CAT), and superoxide dismutase (SOD), while reducing lipid peroxidation (LPO), thereby supporting its antioxidant role. Moreover, d-gal enhanced NF-kB-mediated neuroinflammation, apoptotic markers including caspase-3 and PARP-1, and suppressed synaptic proteins (SNAP-23 and PSD-95). Interestingly, these expression aberrations were reversed upon AA administration. Histological analyses using Nissl and Fluoro-Jade B staining further supported neuronal protection in the cortex and hippocampus. Collectively, these findings suggest that AA exerts neuroprotective effects against d-gal-induced aging and cognitive decline by reducing oxidative stress, neuroinflammation, neuronal apoptosis, and enhancing synaptic plasticity through BDNF/TrkB/Akt/CREB signaling.

Graphical abstract