Evidence map›Paper›PMID 42434808›Full record

ReviewNanomedicine (London, England)2026

Brain targeting and trafficking of extracellular vesicles in central nervous system diseases: a therapeutic roadmap.

Blaine Baker, Samuel Emerson, Taylor Tran, Nikita Mohapatra, David Wang, Thant Zaw, Aaleesha Doshi, Juan-Maria Lopez, Dua Hassan, Priyadarsini Kumar and 2 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nanomedicine (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Blaine BakerCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
Samuel EmersonCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
Taylor TranCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
Nikita MohapatraCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
David WangCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
Thant ZawCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
Aaleesha DoshiCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
Juan-Maria LopezCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
Dua HassanCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
Priyadarsini KumarCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
Diana FarmerCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.
Aijun WangCenter for Bioengineering in Medicine, Davis School of Medicine, University of California, Sacramento, CA, USA.

Funding

NIH HHS 1R01EB033389NIH HHS 1R01EB034279NIH HHS 1R01NS115860NIH HHS 1R01NS131538NIH HHS 1R01NS144390
6 · The paper itself

Abstract

Extracellular vesicles (EVs) mediate intercellular signaling in the central nervous system (CNS) by transferring lipids, proteins, and nucleic acids among neurons, glia, endothelium, and immune cells. Brain targeting depends on a linked sequence: EV ligands and adsorbed protein coronas engage receptor modules, select endocytic routes, determine intracellular fate, and define the therapeutic readouts. These fates include lysosomal degradation, recycling, rare cytosolic delivery, or transport across the blood-brain barrier (BBB). In disease, the same pathways can disseminate proteopathic seeds and amplify neuroinflammation. Heparan sulfate proteoglycans (HSPGs) and LDL receptor family members, including low-density lipoprotein receptor-related protein 1 (LRP1), regulate tau, α-synuclein, and amyloid-β handling. Phosphatidylserine readers and complement shape myeloid sink capture and inflammatory output. Integrin, tetraspanin, and ICAM-1 nanoclusters influence avidity, organotropism, and immune suppression. At the BBB, endothelial HSPGs, LRP1, and transferrin receptor (TfR) support receptor-mediated uptake, motivating engineered ligands such as rabies virus glycoprotein-derived peptides, Angiopep-2, and TfR binders. However, endosomal escape remains a major kinetic barrier to nucleic acid delivery. We synthesize these principles across Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, glioblastoma, and demyelinating disease, and outline design and assay standards needed to translate EV biology into safe, manufacturable CNS therapeutics.

Indexed as

BrainCentral Nervous System DiseasesExtracellular VesiclesAnimalsBlood-Brain BarrierDrug Delivery SystemsHumansLow Density Lipoprotein Receptor-Related Protein-1Low Density Lipoprotein Receptor-Related Protein-1blood-brain barrierendosomal escapeExtracellular vesiclesmicroglianeurodegenerationprotein coronareceptor-mediated transcytosisuptake logic

Identifiers

PMID42434808
PMCPMC13432862

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 Socratic graph.