AB015. Study of microglia in Alzheimer’s disease: chemical structure and modeling of TREM2
Abstract

AB015. Study of microglia in Alzheimer’s disease: chemical structure and modeling of TREM2

Elena Mishina

Cambridge Centre for International Research, Moscow, Russia

Correspondence to: Elena Mishina, BS, BA. Cambridge Centre for International Research, 13 Pavla Korchagina Street, Moscow 129626, Russia. Email: elenamishina1408@gmail.com.

Background: One of the main causes of Alzheimer’s disease is a large accumulation of a protein called beta-amyloid, which later forms into plaques, causing great damage to neurons. The same protein negatively affects the function of microglia, the structure that cleans the blood vessels of the brain of various toxins, thereby protecting our brain from all kinds of pathogens. Too much accumulation of amyloid plaques disrupts microglia, and it begins to kill healthy neurons, leading to neurodegeneration and Alzheimer’s symptoms. However, with genetic modification and boron neutron capture therapy (BNCT), it is possible to fix microglia and prevent neuronal loss in the brain, targeting each beta-amyloid plaque separately to eliminate their further spread. To do this, it is necessary to modify the structure of the microglial receptor, the trigger receptor expressed on myeloid cells 2 (TREM2), which directs microglia function. This study aimed to conduct the computer modulation to find the specific molecules that contribute to the occurrence of mutations in TREM2.

Methods: In this experiment, the three-dimensional (3D) model of TREM2 was created with Python code in PyMOL to demonstrate its cellular structure. Through such computer simulation, it was possible to look at the molecular compounds of the receptor to choose specific genetic therapies that can be applied to modify TREM2. While programming the TREM2 receptor, the author examined its structure and illuminated different colors of the cellular lattice components, backbone, and side chains of the element.

Results: The outcomes of this experiment showed the best approach to manipulate the work of TREM2 for easier navigation of beta-amyloid plaques in the brain for its further treatment through BNCT. By structuring different programs, it was possible to see the molecule that is suggested to play the role of TREM2 trigger agent—interleukin-3 (IL-3).

Conclusions: This study demonstrated the potential that TREM2 modification can play in slowing down the progression of Alzheimer’s disease. The next step would be to promulgate IL-3 molecules, getting rid of the inflammation in the brain cells to normalize the microglia function.

Keywords: Alzheimer’s disease; microglia; neurodegeneration; beta-amyloid plaques; trigger receptor expressed on myeloid cells 2 (TREM2)

Acknowledgments

The author of this article would like to thank Dr. Gonca Bayraktar and Dr. Mehtap Bacioglu from Cambridge Centre for International Research and Harrison Nolan, Director of Innovation in the Knowledge Society, for providing mentorship and feedback throughout the research analysis process.

Footnote

Funding: None.

Conflicts of Interest: The author has completed the ICMJE uniform disclosure form (available at https://tro.amegroups.com/article/view/10.21037/tro-25-ab015/coif). E.M. reported receiving support from the Cambridge Centre for International Research and The Knowledge Society, mainly in the form of guidance during the final stage of the research and access to educational resources. The author has no other conflicts of interest to declare.

Ethical Statement: The author is accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. No human subjects, animal experiments, or clinical data were used in the preparation of this manuscript. As such, ethics approval and informed consent are not applicable.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the noncommercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

doi: 10.21037/tro-25-ab015
Cite this abstract as: Mishina E. AB015. Study of microglia in Alzheimer’s disease: chemical structure and modeling of TREM2. Ther Radiol Oncol 2025;9:AB015.

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