Alzheimer's Research 41 min read January 28, 2026

Lipid Nanoparticles Deliver RNA to the Brain for Alzheimer’s

Lipid Nanoparticles Deliver RNA to the Brain for Alzheimer's

The inhibition of PU.1 using RNA therapy delivered with lipid nanoparticles as a novel treatment for Alzheimer’s disease.

Neurodegenerative disorders are typically linked to chronic neuroinflammation. Alzheimer’s disease (AD) is not an exception since chronic inflammation is one of the hallmarks that contributes to the progression of the disorder.[2] Microglia cells are the main characters in promoting neuroinflammation since they are the most abundant brain immune cells. [2-5] Microglia cells are well known to clear different waste materials from the brain and confer neuroprotection (see Fig.1).[6] However, recent studies have pointed to the presence of AD-risk locus in the microglia genome.[2] AD-risk loci are specific fragments located in the genome that can potentially promote AD development.[3,14] These AD-risk loci open many opportunities for RNA therapeutic methods.[3,6] RNA therapies have been studied for almost all types of disorders, like Parkinson’s disease, AD, and cancer, among others.[3,9,10] The problem with this type of therapy is that it is difficult to find the correct method for transfection, depending on the area or interest. The transfection process, which introduces RNA into cells, is used to modify the host cell genome, changing the cell fate. [10,11] In the case of inhibiting with RNA transfection therapy, the siRNA is used. [2,12] siRNA (small interfering RNA) are small fragments of artificially synthesized RNA capable of inhibiting a specific genome fragment.[10]

Figure 1. Show the roles of the microglia in a healthy brain versus one with Alzheimer’s disease.[6]

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On the other hand, neurodegenerative disorder therapies usually face the obstacle of the blood-brain barrier, and RNA therapy is not excluded.[10,11] Several investigators have studied a novel modality of using lipid nanoparticles (LNPs) to deliver RNA into the brain capable of trespassing the blood-brain barrier for brain cell intake.[1-4] However, recent articles show that injecting the LNPs directly into the brain is the most efficient strategy.[2,14] RNA therapy is usually programmed to target a specific locus in the genome.[4,8] The discovery of several AD-risk loci in the microglia makes them the perfect target for RNA therapy for AD.[2] Some studies demonstrated the efficiency of using LNPs for RNA therapy delivery in the brain.[1-5] According to several investigations, the best route of administration is the local intracisternal injection.[2,14] The local intracisternal injection is directed into the cisterna magna at the base of the skull. Even though the method is considered invasive, different studies show it is highly effective with no extraordinary negative consequences. [2,7,14] RNA therapy can be developed differently depending on the locus of interest. Recently, the investigators identified the PU.1 transcription factor as one of the loci in the microglia. [2,9] The PU.1 transcription factor promotes the progression of AD and neuroinflammation.[9]

For this reason, researchers have developed a novel strategy for using siRNA to target PU.1. [2,9] In this case, the siRNA targets PU.1 in the microglia cells as a therapy for AD. [2] The way it works is by using the LNP called MG-LNP formulation.[2] MG-LNP is a lipid nanoparticle effectively capable of delivering the anti PU.1 siRNA into the microglia cells.[2,9,12] By achieving this delivery, the inhibition of PU.1 in the microglia reduces the promotion of chronic inflammation, thus helping to slow down AD progression (see Fig.2).[9] MG-LNP has been tested in stem cell-derived microglia-like cells (iMGLs) in vitro and in vivo models.[9] MG-LNP proved to be nontoxic and very effective in reducing the expression of PU.1 in microglia cells, thus reducing neuroinflammation.[2,9] In addition, the mechanism of MG-LNP affects not only the microglia cells but astrocytes, which are also known for contributing to the induction of neuroinflammation in AD.[2-4] After some analysis, the investigators found that over 90% of the siRNA successfully transfected the target cells.[2,10-12]

Figure 2. A comparison between stem cell-derived microglia-like cells (iMGLs) treated with LNP + scramble (control group) versus iMGLs treated with LNP+PU.1 siRNA, resulting in a decrease of PU.1 expression.[9]

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Another important fact is that only microglia or astrocytes can take up the siRNA from the MG-LNP.[2] Several investigations show the relationship between chronic neuroinflammation and the progression of AD. [4-6] Different studies show that individuals with higher inflammatory protein levels in the brain tend to develop AD.[4] Neuroinflammation alone has the potential to cause neuronal loss, leading to dementia (see Fig. 1).[6] Inflammation is a natural immune system response.[4,6] Still, the excessive liberation of cytokines (inflammatory promoters) is detrimental. In the case of the brain, chronic neuroinflammation induces the progression of different neurodegenerative disorders, including AD. [4,6] Microglia cells have been studied intensely in recent years to identify AD-risk loci.[2] These findings opened the window for new ways of targeting AD. The presence of the PU.1 transcription factor in the microglia represents an opportunity for siRNA therapy to inhibit the expression of this inflammatory promotor. [1-3]

The inhibition of PU.1 using siRNA technology slows AD progression by decreasing the chronic inflammation that characterizes AD. [1-3] LNP delivery is an emerging way of treating different disorders, including neurodegeneration. [2-5] MG-LNP effectively delivered up to 90% of the siRNA anti-PU. 1.[2,10-12] The inhibition of the PU.1 transcription factor is well known to help neuroprotection and improve cognitive function.[6] In general terms, lipid nanoparticles have exhibited promising results in treating AD.[1] LNPs can deliver drugs and other therapeutic agents across the blood-brain barrier.[1,4-7] LNPs have low toxicity and are easy to modify, and the cells absorb them without problem. LNPs are a competitive technology for treating AD and other neurodegenerative disorders. More investigations need to be done to evaluate the potential of creating multitargeting therapies.

References

[Barriga, H. M., Pence, I. J., Holme, M. N., Doutch, J. J., Penders, J., Nele, V., ... & Stevens, M. M. (2022). Coupling Lipid Nanoparticle Structure and Automated Single‐Particle Composition Analysis to Design Phospholipase‐Responsive Nanocarriers. _Advanced Materials_, _34_(26), 2200839.](https://doi.org/10.1002/adma.202200839 "Coupling Lipid Nanoparticle Structure and Automated Single-Particle Composition Analysis to Design Phospholipase-Responsive Nanocarriers")
[Guo, S., Cázarez-Márquez, F., Jiao, H., Foppen, E., Korpel, N. L., Grootemaat, A. E., ... & Yi, C. X. (2022). Specific silencing of microglial gene expression in the rat brain by nanoparticle-based small interfering RNA delivery. _ACS applied materials & interfaces_, _14_(4), 5066-5079.](https://doi.org/10.1021/acsami.1c22434 "Specific Silencing of Microglial Gene Expression in the Rat Brain by Nanoparticle-Based Small Interfering RNA Delivery")
[Jung, H. N., Lee, S. Y., Lee, S., Youn, H., & Im, H. J. (2022). Lipid nanoparticles for delivery of RNA therapeutics: Current status and the role of in vivo imaging. _Theranostics_, _12_(17), 7509.](https://doi.org/10.7150%2Fthno.77259 "Lipid nanoparticles for delivery of RNA therapeutics: Current status and the role of in vivo imaging")
[Kim, S. S., Ye, C., Kumar, P., Chiu, I., Subramanya, S., Wu, H., ... & Manjunath, N. (2010). Targeted delivery of siRNA to macrophages for anti-inflammatory treatment. _Molecular therapy_, _18_(5), 993-1001.](https://doi.org/10.1038/mt.2010.27 "Targeted delivery of siRNA to macrophages for anti-inflammatory treatment")
[Lau, S. F., Chen, C., Fu, W. Y., Qu, J. Y., Cheung, T. H., Fu, A. K., & Ip, N. Y. (2020). IL-33-PU. One transcriptome reprogramming drives functional state transition and clearance activity of microglia in Alzheimer’s disease: c _ell Reports_, _31_(3).](https://doi.org/10.1016/j.celrep.2020.107530 "IL-33-PU.1 Transcriptome Reprogramming Drives Functional State Transition and Clearance Activity of Microglia in Alzheimer's Disease")
Miao, J., Ma, H., Yang, Y., Liao, Y., Lin, C., Zheng, J., ... & Lan, J. (2023). Microglia in Alzheimer’s disease: pathogenesis, mechanisms, and therapeutic potentials. Frontiers in Aging Neuroscience, 15, 1201982.
[Ndeupen, S., Qin, Z., Jacobsen, S., Bouteau, A., Estanbouli, H., & Igyártó, B. Z. (2021). The mRNA-LNP platform's lipid nanoparticle component used in preclinical vaccine studies is highly inflammatory.Iscience, 24(12).](https://doi.org/10.1016/j.isci.2021.103479 "The mRNA-LNP platform's lipid nanoparticle component used in preclinical vaccine studies is highly inflammatory")
Novikova, G., Kapoor, M., Tcw, J., Abud, E. M., Efthymiou, A. G., Chen, S. X., ... & Goate, A. M. (2021). Integration of Alzheimer’s disease genetics and myeloid genomics identifies disease risk regulatory elements and genes. _Nature communications_, _12_(1), 1610.
[Ralvenius, W. T., Andresen, J. L., Huston, M. M., Penney, J., Bonner, J. M., Fenton, O. S., ... & Tsai, L. H. (2023). Nanoparticle‐mediated delivery of Anti‐PU. One siRNA via localized intracisternal administration reduces neuroinflammation. _Advanced Materials_, 2309225.](https://doi.org/10.1002/adma.202309225 "Nanoparticle-Mediated Delivery of Anti-PU.1 siRNA via Localized Intracisternal Administration Reduces Neuroinflammation")
[Rungta, R. L., Choi, H. B., Lin, P. J., Ko, R. W., Ashby, D., Nair, J., ... & MacVicar, B. A. (2013). Lipid nanoparticle delivery of siRNA to silence neuronal gene expression in the brain. _Molecular therapy. Nucleic acids_, _2_(12), e136.](https://doi.org/10.1038%2Fmtna.2013.65 "Lipid Nanoparticle Delivery of siRNA to Silence Neuronal Gene Expression in the Brain")
[Rungta, R. L., Choi, H. B., Lin, P. J., Ko, R. W., Ashby, D., Nair, J., ... & MacVicar, B. A. (2013). Lipid nanoparticle delivery of siRNA to silence neuronal gene expression in the brain. _Molecular therapy. Nucleic acids_, _2_(12), e136.](https://doi.org/10.1038/mtna.2013.65 "Lipid Nanoparticle Delivery of siRNA to Silence Neuronal Gene Expression in the Brain")
[Rustenhoven, J., Smith, A. M., Smyth, L. C., Jansson, D., Scotter, E. L., Swanson, M. E., ... & Dragunow, M. (2018). PU. 1 regulates Alzheimer’s disease-associated genes in primary human microglia. _Molecular neurodegeneration_, _13_(1), 1-16.](https://doi.org/10.1186/s13024-018-0277-1 "PU.1 regulates Alzheimer's disease-associated genes in primary human microglia")
[Tsakiri, M., Zivko, C., Demetzos, C., & Mahairaki, V. (2022). Lipid-based nanoparticles and RNA as innovative neuro-therapeutics. _Frontiers in Pharmacology_, _13_, 900610.](https://doi.org/10.3389/fphar.2022.900610 "Lipid-based nanoparticles and RNA as innovative neuro-therapeutics")
[Tuma, J., Chen, Y. J., Collins, M. G., Paul, A., Li, J., Han, H., ... & Lee, H. Y. (2023). Lipid nanoparticles deliver mRNA to the brain after an intracerebral injection. _Biochemistry_, _62_(24), 3533-3547.](https://doi.org/10.1021/acs.biochem.3c00371 "Lipid Nanoparticles Deliver mRNA to the Brain after an Intracerebral Injection")

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