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<p>Extensive evidence suggests overlapping pathological mechanisms in the brain of individuals with Parkinson’s disease dementia, Down syndrome dementia, and Alzheimer’s disease. For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). Subsequently, we performed a transcriptomic analysis that corrected for the transcriptional age in the hippocampus of affected individuals, highlighting common underlying pathogenic mechanisms. There were 45 common differentially expressed genes (DEGs), whereas enriched functional terms were related to lysine <i>N</i>-methyltransferase activity and intermediate filament. Co-expression network analysis displayed a module that was significantly downregulated in the non-demented control group only. This module identified <i>EHMT2</i> and <i>LMNB2</i> as hub genes, which were also common DEGs. Overall, these findings uncover shared functional insights in the hippocampus, while specifically highlighting <i>EHMT2</i> and <i>LMNB2</i> as potential universal biomarkers or disease-altered targets across neurodegenerative dementias.</p>

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Common pathogenic mechanisms in the hippocampus across neurodegenerative dementias: Alzheimer’s disease, Down syndrome, and Parkinson’s disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月29日

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  • René A. J. Crans,
  • Marta Fructuoso,
  • Karen Bascón-Cardozo,
  • Hatice Recaioglu,
  • Jesus Sotelo-Fonseca,
  • Yannick Vermeiren,
  • André Strydom,
  • Debby Van Dam,
  • Peter P. De Deyn,
  • Bernardo Rodríguez-Martín,
  • Marie-Claude Potier,
  • Mara Dierssen

摘要

Extensive evidence suggests overlapping pathological mechanisms in the brain of individuals with Parkinson’s disease dementia, Down syndrome dementia, and Alzheimer’s disease. For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). Subsequently, we performed a transcriptomic analysis that corrected for the transcriptional age in the hippocampus of affected individuals, highlighting common underlying pathogenic mechanisms. There were 45 common differentially expressed genes (DEGs), whereas enriched functional terms were related to lysine N-methyltransferase activity and intermediate filament. Co-expression network analysis displayed a module that was significantly downregulated in the non-demented control group only. This module identified EHMT2 and LMNB2 as hub genes, which were also common DEGs. Overall, these findings uncover shared functional insights in the hippocampus, while specifically highlighting EHMT2 and LMNB2 as potential universal biomarkers or disease-altered targets across neurodegenerative dementias.