Alzheimer's Disease and Adult Hippocampal Neurogenesis: Tracking Aβ and Immature Neuron Markers

Research Article
Open access

Alzheimer's Disease and Adult Hippocampal Neurogenesis: Tracking Aβ and Immature Neuron Markers

Zhengyang Xu 1*
  • 1 Department of Chemistry, University of Washington, Seattle, WA, 98195-2700, USA    
  • *corresponding author zx062504@uw.edu
Published on 20 June 2025 | https://doi.org/10.54254/2753-8818/2025.24201
TNS Vol.116
ISSN (Print): 2753-8826
ISSN (Online): 2753-8818
ISBN (Print): 978-1-80590-197-6
ISBN (Online): 978-1-80590-198-3

Abstract

From the work of Moreno-Jimenez et al., it is known that the generation of new neurons dramatically declines in patients with Alzheimer’s disease compared with mentally healthy individuals, marked by DCX+ cells (immature neurons) failing to produce other structures characteristic of mature neurons. The same researchers also observed that such a phenomenon worsened as Alzheimer’s disease progressed but did not offer any explanation. This research proposal introduces an experiment that could reveal the mechanism behind the decrease of adult hippocampal neurogenesis in patients with Alzheimer’s disease. Focusing on Aβ1-42, a hallmark of Alzheimer’s disease, this paper examines its role in reducing the number of new neurons produced. Techniques such as immunofluorescence, chromatin immunoprecipitation sequencing, and RNA sequencing are employed.

Keywords:

Alzheimer’s disease, Aβ, Adult hippocampal neurogenesis, Neuron markers

Xu,Z. (2025). Alzheimer's Disease and Adult Hippocampal Neurogenesis: Tracking Aβ and Immature Neuron Markers. Theoretical and Natural Science,116,13-17.
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References

[1]. Breijyeh, Z., & Karaman, R. (2020). Comprehensive review on Alzheimer’s disease: Causes and treatment. Molecules, 25(24), 5789. https://doi.org/10.3390/molecules25245789

[2]. Moreno-Jiménez, E. P., Flor-García, M., Terreros-Roncal, J., Rábano, A., Cafini, F., Pallas-Bazarra, N., Ávila, J., & Llorens-Martín, M. (2019). Adult hippocampal neurogenesis is abundant in neurologically healthy subjects and drops sharply in patients with Alzheimer’s disease. Nature Medicine, 25(4), 554–560. https://doi.org/10.1038/s41591-019-0375-9

[3]. Cao, Y., Liu, P., Bian, H., Jin, S., Liu, J., Yu, N., Cui, H., Sun, F., Qian, X., Qiu, W., & Ma, C. (2023). Reduced neurogenesis in human hippocampus with Alzheimer’s disease. Brain Pathology, 34(3). https://doi.org/10.1111/bpa.13225

[4]. Barucker, C., Harmeier, A., Weiske, J., Fauler, B., Albring, K. F., Prokop, S., Hildebrand, P., Lurz, R., Heppner, F. L., Huber, O., & Multhaup, G. (2014). Nuclear translocation uncovers the amyloid peptide AΒ42 as a regulator of gene transcription*. Journal of Biological Chemistry, 289(29), 20182–20191. https://doi.org/10.1074/jbc.m114.564690

[5]. Hampel, H., Hardy, J., Blennow, K., Chen, C., Perry, G., Kim, S. H., Villemagne, V. L., Aisen, P., Vendruscolo, M., Iwatsubo, T., Masters, C. L., Cho, M., Lannfelt, L., Cummings, J. L., & Vergallo, A. (2021). The amyloid-Β pathway in Alzheimer’s disease. Molecular Psychiatry, 26(10), 5481–5503. https://doi.org/10.1038/s41380-021-01249-0

[6]. Hayden, E. Y., & Teplow, D. B. (2013). Amyloid β-protein oligomers and Alzheimer’s disease. Alzheimer S Research & Therapy, 5(6), 60. https://doi.org/10.1186/alzrt226

[7]. Texari, L., Spann, N. J., Troutman, T. D., Sakai, M., Seidman, J. S., & Heinz, S. (2021). An optimized protocol for rapid, sensitive and robust on-bead ChIP-seq from primary cells. STAR Protocols, 2(1), 100358. https://doi.org/10.1016/j.xpro.2021.100358

[8]. Koch, C. M., Chiu, S. F., Akbarpour, M., Bharat, A., Ridge, K. M., Bartom, E. T., & Winter, D. R. (2018). A Beginner’s Guide to analysis of RNA sequencing data. American Journal of Respiratory Cell and Molecular Biology, 59(2), 145–157. https://doi.org/10.1165/rcmb.2017-0430tr

[9]. Akyuva, Y., Nazıroğlu, M., & Yıldızhan, K. (2020). Selenium prevents interferon-gamma induced activation of TRPM2 channel and inhibits inflammation, mitochondrial oxidative stress, and apoptosis in microglia. Metabolic Brain Disease, 36(2), 285–298. https://doi.org/10.1007/s11011-020-00624-0

[10]. Monteiro, A. R., Barbosa, D. J., Remião, F., & Silva, R. (2023). Alzheimer’s disease: Insights and new prospects in disease pathophysiology, biomarkers and disease-modifying drugs. Biochemical Pharmacology, 211, 115522. https://doi.org/10.1016/j.bcp.2023.115522

Cite this article

Xu,Z. (2025). Alzheimer's Disease and Adult Hippocampal Neurogenesis: Tracking Aβ and Immature Neuron Markers. Theoretical and Natural Science,116,13-17.

Data availability

The datasets used and/or analyzed during the current study will be available from the authors upon reasonable request.

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About volume

Volume title: Proceedings of the 3rd International Conference on Modern Medicine and Global Health

ISBN：978-1-80590-197-6(Print) / 978-1-80590-198-3(Online)
Editor：Sheiladevi Sukumaran
Conference website: https://2025.icmmgh.org/
Conference date: 20 January 2025
Series: Theoretical and Natural Science
Volume number: Vol.116
ISSN：2753-8818(Print) / 2753-8826(Online)

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References

[1]. Breijyeh, Z., & Karaman, R. (2020). Comprehensive review on Alzheimer’s disease: Causes and treatment. Molecules, 25(24), 5789. https://doi.org/10.3390/molecules25245789

[2]. Moreno-Jiménez, E. P., Flor-García, M., Terreros-Roncal, J., Rábano, A., Cafini, F., Pallas-Bazarra, N., Ávila, J., & Llorens-Martín, M. (2019). Adult hippocampal neurogenesis is abundant in neurologically healthy subjects and drops sharply in patients with Alzheimer’s disease. Nature Medicine, 25(4), 554–560. https://doi.org/10.1038/s41591-019-0375-9

[3]. Cao, Y., Liu, P., Bian, H., Jin, S., Liu, J., Yu, N., Cui, H., Sun, F., Qian, X., Qiu, W., & Ma, C. (2023). Reduced neurogenesis in human hippocampus with Alzheimer’s disease. Brain Pathology, 34(3). https://doi.org/10.1111/bpa.13225

[4]. Barucker, C., Harmeier, A., Weiske, J., Fauler, B., Albring, K. F., Prokop, S., Hildebrand, P., Lurz, R., Heppner, F. L., Huber, O., & Multhaup, G. (2014). Nuclear translocation uncovers the amyloid peptide AΒ42 as a regulator of gene transcription*. Journal of Biological Chemistry, 289(29), 20182–20191. https://doi.org/10.1074/jbc.m114.564690

[5]. Hampel, H., Hardy, J., Blennow, K., Chen, C., Perry, G., Kim, S. H., Villemagne, V. L., Aisen, P., Vendruscolo, M., Iwatsubo, T., Masters, C. L., Cho, M., Lannfelt, L., Cummings, J. L., & Vergallo, A. (2021). The amyloid-Β pathway in Alzheimer’s disease. Molecular Psychiatry, 26(10), 5481–5503. https://doi.org/10.1038/s41380-021-01249-0

[6]. Hayden, E. Y., & Teplow, D. B. (2013). Amyloid β-protein oligomers and Alzheimer’s disease. Alzheimer S Research & Therapy, 5(6), 60. https://doi.org/10.1186/alzrt226

[7]. Texari, L., Spann, N. J., Troutman, T. D., Sakai, M., Seidman, J. S., & Heinz, S. (2021). An optimized protocol for rapid, sensitive and robust on-bead ChIP-seq from primary cells. STAR Protocols, 2(1), 100358. https://doi.org/10.1016/j.xpro.2021.100358

[8]. Koch, C. M., Chiu, S. F., Akbarpour, M., Bharat, A., Ridge, K. M., Bartom, E. T., & Winter, D. R. (2018). A Beginner’s Guide to analysis of RNA sequencing data. American Journal of Respiratory Cell and Molecular Biology, 59(2), 145–157. https://doi.org/10.1165/rcmb.2017-0430tr

[9]. Akyuva, Y., Nazıroğlu, M., & Yıldızhan, K. (2020). Selenium prevents interferon-gamma induced activation of TRPM2 channel and inhibits inflammation, mitochondrial oxidative stress, and apoptosis in microglia. Metabolic Brain Disease, 36(2), 285–298. https://doi.org/10.1007/s11011-020-00624-0

[10]. Monteiro, A. R., Barbosa, D. J., Remião, F., & Silva, R. (2023). Alzheimer’s disease: Insights and new prospects in disease pathophysiology, biomarkers and disease-modifying drugs. Biochemical Pharmacology, 211, 115522. https://doi.org/10.1016/j.bcp.2023.115522

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