Evidence map›Paper›PMID 30541599›Full record

ArticleFluids and barriers of the CNS2018

Choroid plexus genes for CSF production and brain homeostasis are altered in Alzheimer's disease.

Shawn Kant, Edward G Stopa, Conrad E Johanson, Andrew Baird, Gerald D Silverberg

Open access · goldAbstract read
In one paragraph

Article in Fluids and barriers of the CNS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 7% of its field
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

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Choroid Plexus Abnormalities in Autoimmune Encephalitis.CNS neuroscience & therapeutics · 2026
    Article
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  7. Choroid plexus remodeling linked to impaired CSF-mediated clearance and Alzheimer's disease progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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6 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Shawn KantDepartment of Pathology (Neuropathology Division), Warren Alpert Medical School at Brown University, Providence, RI, 02903, USA.
Edward G StopaDepartment of Pathology (Neuropathology Division), Warren Alpert Medical School at Brown University, Providence, RI, 02903, USA.
Conrad E JohansonDepartment of Neurosurgery, Warren Alpert Medical School at Brown University, Providence, RI, 02903, USA.
Andrew BairdDepartment of Surgery, University of California San Diego, La Jolla, CA, USA.
Gerald D SilverbergDepartment of Neurosurgery, Stanford University, 710 Frenchmans Rd, Stanford, CA, 94305, USA. geralds@stanford.edu.
Brown University · USStanford University · USUniversity of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe roles of the choroid plexus (CP) and cerebrospinal fluid (CSF) production have drawn increasing attention in Alzheimer's disease (AD) research. Specifically, studies document markedly decreased CSF production and turnover in moderate-to-severe AD. Moreover, reduced CP function and CSF turnover lead to impaired clearance of toxic metabolites, likely promote neuroinflammation, and may facilitate neuronal death during AD progression. We analyzed CP gene expression in AD compared with control subjects, specifically considering those genes involved with CSF production and CP structural integrity.

methodsThe Brown-Merck Gene Expression Omnibus (GEO) database (CP transcripts) was mined to examine changes in gene expression in AD compared to controls with a focus on assorted genes thought to play a role in CSF production. Specifically, genes coding for ion transporters in CP epithelium (CPE) and associated enzymes like Na-K-ATPase and carbonic anhydrase, aquaporins, mitochondrial transporters/enzymes, blood-cerebrospinal fluid barrier (BCSFB) stability proteins, and pro-inflammatory mediators were selected for investigation. Data were analyzed using t test p-value and fold-change analysis conducted by the GEO2R feature of the GEO database.

resultsSignificant expression changes for several genes were observed in AD CP. These included disruptions to ion transporters (e.g., the solute carrier gene SLC4A5, p = 0.004) and associated enzyme expressions (e.g., carbonic anhydrase CA4, p = 0.0001), along with decreased expression of genes involved in BCSFB integrity (e.g., claudin CLDN5, p = 0.039) and mitochondrial ATP synthesis (e.g., adenosine triphosphate ATP5L, p = 0.0004). Together all changes point to disrupted solute transport at the blood-CSF interface in AD. Increased expression of pro-inflammatory (e.g., interleukin IL1RL1, p = 0.00001) and potential neurodegenerative genes (e.g., amyloid precursor APBA3, p = 0.002) also implicate disturbed CP function.

conclusionsBecause the altered expression of numerous transcripts in AD-CP help explain decreased CSF production in AD, these findings represent a first step towards identifying novel therapeutic targets in AD.

Indexed as

Alzheimer DiseaseBlood-Brain BarrierBrainChoroid PlexusDatabases, FactualGene ExpressionGene Expression ProfilingHomeostasisHumansIon TransportBarrier permeabilityBeta amyloidBlood–brain barrierBlood–CSF barrierChoroidal tight junctionsChoroid plexus Gene Expression OmnibusChoroid plexus transcriptomeCSF productionHomeostasisMitochondriaSolute carrier families

Identifiers

PMID30541599
PMCPMC6291926
OpenAlexW2905072897

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.