Evidence map›Paper›PMID 39357152›Full record

ArticleBiomaterials2025

Engineered 3D human neurovascular model of Alzheimer's disease to study vascular dysfunction.

Georgios Pavlou, Sarah Spitz, Francesca Michela Pramotton, Alice Tsai, Brent M Li, Xun Wang, Olivia M Barr, Eunkyung Clare Ko, Shun Zhang, Savannah J Ashley and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomaterials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
–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

25 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. A cerebrospinal fluid blood-brain barrier dysfunction score is associated with progression from mild cognitive impairment to Alzheimer's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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  17. Nephroprotective Effect ofInternational journal of molecular sciences · 2025
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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

15 authors.

Georgios PavlouDepartment of Mechanical Engineering and Biological Engineering, Massachusetts Institute of Technology, Cambridge MA, 02139, USA.
Sarah SpitzDepartment of Mechanical Engineering and Biological Engineering, Massachusetts Institute of Technology, Cambridge MA, 02139, USA.
Francesca Michela PramottonDepartment of Mechanical Engineering and Biological Engineering, Massachusetts Institute of Technology, Cambridge MA, 02139, USA.
Alice TsaiGenetics and Aging Research Unit, McCance Center for Brain Health, Mass General Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA.
Brent M LiGenetics and Aging Research Unit, McCance Center for Brain Health, Mass General Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA.
Xun WangDepartment of Mechanical Engineering and Biological Engineering, Massachusetts Institute of Technology, Cambridge MA, 02139, USA.
Olivia M BarrGenetics and Aging Research Unit, McCance Center for Brain Health, Mass General Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA.
Eunkyung Clare KoDepartment of Mechanical Engineering and Biological Engineering, Massachusetts Institute of Technology, Cambridge MA, 02139, USA.
Shun ZhangDepartment of Mechanical Engineering and Biological Engineering, Massachusetts Institute of Technology, Cambridge MA, 02139, USA.
Savannah J AshleyDepartment of Mechanical Engineering and Biological Engineering, Massachusetts Institute of Technology, Cambridge MA, 02139, USA.
Anna Maaser-HeckerGenetics and Aging Research Unit, McCance Center for Brain Health, Mass General Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA.
Se Hoon ChoiGenetics and Aging Research Unit, McCance Center for Brain Health, Mass General Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA.
Mehdi JorfiGenetics and Aging Research Unit, McCance Center for Brain Health, Mass General Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA. Electronic address: mjorfi@mgh.harvard.edu.
Rudolph E TanziGenetics and Aging Research Unit, McCance Center for Brain Health, Mass General Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA. Electronic address: tanzi@helix.mgh.harvard.edu.
Roger D KammDepartment of Mechanical Engineering and Biological Engineering, Massachusetts Institute of Technology, Cambridge MA, 02139, USA. Electronic address: rdkamm@mit.edu.

Funding

Human 3D Neuro-Vascular Interaction and Meningeal Lymphatic Models with Application to Alzheimer’s DiseaseR01NS121078 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI CHOI, SE HOON, JORFI, MEHDI · 2021 to 2025
$2.6M
NINDS NIH HHS R01 NS121078
6 · The paper itself

Abstract

The blood-brain barrier (BBB) serves as a selective filter that prevents harmful substances from entering the healthy brain. Dysfunction of this barrier is implicated in several neurological diseases. In the context of Alzheimer's disease (AD), BBB breakdown plays a significant role in both the initiation and progression of the disease. This study introduces a three-dimensional (3D) self-assembled in vitro model of the human neurovascular unit to recapitulate some of the complex interactions between the BBB and AD pathologies. It incorporates primary human brain endothelial cells, pericytes and astrocytes, and stem cell-derived neurons and astrocytes harboring Familial AD (FAD) mutations. Over an extended co-culture period, the model demonstrates increased BBB permeability, dysregulation of key endothelial and pericyte markers, and morphological alterations mirroring AD pathologies. The model enables visualization of amyloid-beta (Aβ) accumulation in both neuronal and vascular compartments. This model may serve as a versatile tool for neuroscience research and drug development to provide insights into the dynamic relationship between vascular dysfunction and AD pathogenesis.

Indexed as

Alzheimer DiseaseBlood-Brain BarrierCoculture TechniquesEndothelial CellsAmyloid beta-PeptidesAstrocytesCells, CulturedHumansModels, BiologicalNeuronsPericytesTissue EngineeringAmyloid beta-PeptidesAlzheimer's diseaseAmyloid-βBlood-brain barrierNeurovascular unitPerfusable 3D brain in vitro model

Identifiers

PMID39357152
PMCPMC12012383

What Socratic holds

Textmetadata
LicenceTDM
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.