Dual strategy for Alzheimer's therapy: Peptide screening and nasal nebulizer delivery

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About This Project

Alzheimer’s disease is linked to toxic beta-amyloid 42 (Aβ42) clumps in the brain. Designed peptides can bind to Aβ42 to prevent aggregation. Our approach improves this by using a peptide that not only stops clumping but also helps clear Aβ42 through the body’s natural system. We hypothesize that using a nasal ultrasonic nebulizer to deliver the peptide in the mist will allow it to reach the brain quicker. This innovative method offers a more effective and accessible Alzheimer’s treatment.

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What is the context of this research?

Alzheimer’s disease is driven by the accumulation of toxic amyloid-beta 42, which disrupt neural function, trigger inflammation, and lead to cognitive decline. These aggregates form plaques that interfere with cell signaling and contribute to neuronal death. Our approach develops a functional peptide (https://doi.org/10.1039/D0RA02009E) designed to inhibit and degrade Aβ42 aggregates, addressing both aggregation and clearance. To enhance delivery, we propose using a nasal ultrasonic nebulizer, which bypasses the blood-brain barrier and delivers the peptide directly to the brain. This method improves treatment efficiency, reduces side effects, and provides a cost-effective alternative for early-stage Alzheimer’s patients. Ultimately, our research lays the foundation for more effective, sustainable, and patient-friendly Alzheimer’s therapies.

What is the significance of this project?

Alzheimer’s disease affects approximately 50 million people(https://www.thelancet.com/jour...) worldwide, and its significance is increasing with the aging population. Current treatments, like antibody drugs, have limited effectiveness, struggle with high costs, making them inaccessible to many patients. This research offers a novel solution by developing functional peptides that inhibit and break down amyloid-beta 42 (Aβ42) aggregates, a major contributor to AD progression. Additionally, a nasal nebulizer ensures direct brain delivery, bypassing the blood-brain barrier for faster, safer, and more efficient absorption. By combining targeted therapy with an innovative delivery system, this approach has the potential to improve patient outcomes, reduce costs, and provide a more widely accessible treatment option for millions of families affected by AD.

What are the goals of the project?

Our research aims to develop an innovative Alzheimer’s treatment by establishing two key components: (1) screening and validating four functional peptides designed to inhibit and decompose amyloid beta-42, and (2) developing a nasal nebulizer-based delivery system to bypass the blood-brain barrier. We will synthesize these four peptide candidates and evaluate their ability to bind amyloid beta-42 through in vitro assays. Structural interactions will be assessed using computational modeling and biochemical binding assays. The most effective peptide will be encapsulated in liposomes or other formulations for nasal delivery using an ultrasonic nebulizer, optimizing particle size and stability. Our study will focus on in vitro validation, and no animal or human studies will be conducted at this stage. By systematically testing both peptide function and delivery efficiency, this project will provide critical data on the feasibility of this dual-strategy approach for Alzheimer’s treatment.

Budget

Experimental materials cost
$2,500
Peptide Synthesis Cost
$2,500
Ultrasonic nebulizer prototype development cost
$2,500
Experimental labor costs
$5,000
Cost of in vitro testing
$2,500

1. Experimental Materials: Funding for essential reagents and tools needed to synthesize and test peptides that inhibit amyloid beta 42 aggregation.

2. Peptide Synthesis: Design, synthesize, purify, and analyze peptides as key therapeutic components.

3. Ultrasonic Nebulizer Prototype: Develop a prototype that effectively delivers peptides into the brain via the nasal passages.

4. Labor: Supporting investigators and assistants ensures professional and timely experiments.

5. In Vitro Testing: Investigate the effectiveness of peptides in cell models.

Endorsed by

I support this experiment. It will lead to advancements in the formulation of Alzheimer's disease drugs.

Project Timeline

In the first 1.5 months, we will synthesize and test four peptide candidates for amyloid beta-42 binding. The next 2.5 months will focus on optimizing the nasal ultrasonic nebulizer for efficient peptide delivery. By months 5-7, in vitro studies will evaluate peptide efficacy, with refinements as needed. The final months 8-10 will focus on safety assessments and formulation improvements.

Regular updates will be shared, ensuring backers stay informed on progress, challenges, and key findings.

Mar 09, 2025

Project Launched

Apr 15, 2025

Peptide Synthesis and Binding Characterization Completed

Jun 30, 2025

Ultrasonic Nebulizer Optimized for Peptide Delivery

Sep 30, 2025

In vitro Efficacy Confirmed

Dec 31, 2025

Final Data Analysis and Report Published

Meet the Team

Hyunho Shin
Hyunho Shin
Individual researcher

Affiliates

NOCTUA BIO (a one-person research company)
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Hyunho Shin

Korea Disease Control and Prevention Agency 2005.02 ~ 2008.03

Foodmus H&S Research Institute 2008.03 ~ 2011.07

Ewha Womans University Industry-Academic Cooperation Foundation 2011.10 ~ 2013.03

Hanwha Hotels & Resorts Co., Ltd. 2013.02 ~ 2016.04

DIYBio Lab 2016.05 ~ 2017.02

Korea University College of Medicine 2016.09 ~ 2017.02

Korea Bureau Veritas Co., Ltd. 2017.03 ~ 2023.07

Noctuabio 2023.11 ~ Currently employed

Currently, at Noctuabio, I am leveraging my experience to focus on cutting-edge biotechnology research, particularly in therapeutic development. My professional journey demonstrates adaptability, interdisciplinary collaboration, and a strong dedication to improving public health through science and innovation.


Additional Information

Reference

(1) Masters, C. L., Simms, G., Weinman, N. A., Multhaup, G., McDonald, B. L., & Beyreuther, K. (1985). Amyloid plaque core protein in Alzheimer disease and Down syndrome. Proceedings of the National Academy of Sciences, 82(12), 4245-4249. https://doi.org/10.1073/pnas.82.12.4245 > Amyloid beta 42 is the cause of Alzheimer's

(2) Tang, Y., Xie, J., Xie, W., & Xie, W. (2020). N-Amino peptide scanning reveals inhibitors of Aβ42 aggregation. RSC Advances, 10(20), 11782-11789. https://doi.org/10.1039/D0RA02009E > Functional peptide binds to the hydrophobic portion of amyloid beta 42 and inhibits aggregation

(3) Chang, W., Kim, S., Lee, J., & Park, S. (2021). Intranasal delivery of anti‑tau antibody reduces tau pathology in a mouse model of tauopathy. Scientific Reports, 11, 88264. https://pubmed.ncbi.nlm.nih.go > The content that tau protein antibodies were injected through the nose


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