Evidence map›Paper›PMID 41613446›Full record

ArticleFundamental research2025

Significant downregulation of Alzheimer's amyloid-β levels enabled by engineered DNA nanomaterials.

Yao Sun, Jing Sun, Yang Feng, Yi Zhang, Jingjing Li, Fan Wang, Mark Loznik, Yang Tian, Hongjie Zhang, Andreas Herrmann and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Fundamental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Bio-Inspired and Protein-Based Elastomeric Materials.Polymer science & technology (Washington, D.C.) · 2026
    Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Yao SunEngineering Research Center of Advanced Rare Earth Materials, Department of Chemistry, Tsinghua University, Beijing 100084, China.
Jing SunShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200241, China.
Yang FengGenetics and Aging Research Unit, McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
Yi ZhangState Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China.
Jingjing LiState Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China.
Fan WangState Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China.
Mark LoznikDWI-Leibniz Institute for Interactive Materials, 52056 Aachen, Germany.
Yang TianShanghai Engineering Research Center of Molecular Therapeutics and New Drug Development, School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200241, China.
Hongjie ZhangEngineering Research Center of Advanced Rare Earth Materials, Department of Chemistry, Tsinghua University, Beijing 100084, China.
Andreas HerrmannDWI-Leibniz Institute for Interactive Materials, 52056 Aachen, Germany.
Kai LiuEngineering Research Center of Advanced Rare Earth Materials, Department of Chemistry, Tsinghua University, Beijing 100084, China.
Can ZhangGenetics and Aging Research Unit, McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although there are no effective therapies to block or reverse Alzheimer's disease (AD) progression at present, a promising therapeutic strategy is to reduce levels of amyloid-β (Aβ) proteins, which drive the formation of amyloid plaque, a primary hallmark in AD brains. Herein, we report that amphiphilic lipid-DNA molecules (LD) were designed by incorporating a long alkyl chain into the nucleotide base. It significantly down-regulated Alzheimer's Aβ levels in vivo and in vitro. In contrast to small-molecule chemical drugs and antibody therapies, the assembled DNA nanoparticles allowed them to effectively cross the blood-brain barrier (BBB) and accumulate in the brain, increasing the therapeutic effects. Notably, lipid-DNA downregulated the levels of Aβ peptides significantly in vitro. AD mice model experiments demonstrated that the LD-treated groups exhibited a rapid cognition behavioral improvement, which was associated with brain engagement of LD and reduced Aβ levels. Thus, the molecularly engineered DNA nanomaterials effectively regulated Aβ peptides. This work might provide a promising DNA engineering strategy for AD treatment.

Indexed as

Alzheimer's diseaseAmyloid-β levelDNA nanomaterialDownregulatingMolecular engineering

Identifiers

PMID41613446
PMCPMC12848132

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.