Evidence map›Paper›PMID 32948022›Full record

ReviewPharmaceutics2020

Drugs Modulating CD4+ T Cells Blood-Brain Barrier Interaction in Alzheimer's Disease.

Norwin Kubick, Patrick C Henckell Flournoy, Ana-Maria Enciu, Gina Manda, Michel-Edwar Mickael

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.3field-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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  6. Frontiers in immunology · 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

5 authors at 3 institutions in 3 countries.

Norwin KubickInstitute of Biochemistry, Molecular Cell Biology, University Clinic Hamburg-Eppendorf, 20251 Hamburg, Germany.ORCID 0000-0001-8958-0352
Patrick C Henckell FlournoyPM Research Center, 20 Kaggeholm, Ekerö, 178 54 Stockholm, Sweden.
Ana-Maria EnciuVictor Babes National Institute of Pathology, 050096 București, Romania.ORCID 0000-0002-8122-1096
Gina MandaVictor Babes National Institute of Pathology, 050096 București, Romania.ORCID 0000-0002-9706-1883
Michel-Edwar MickaelBevill Biomedical Sciences Research Building, UAB Birmingham, AL 35294-2170, USA.ORCID 0000-0002-4186-4900
Institutul National Victor Babes · ROInstitute of Genetics and Animal Biotechnology of the Polish Academy of Sciences · PLUniversität Hamburg · DE

Funding

Redbrain P_37_732/2016
6 · The paper itself

Abstract

The effect of Alzheimer's disease (AD) medications on CD4+ T cells homing has not been thoroughly investigated. CD4+ T cells could both exacerbate and reduce AD symptoms based on their infiltrating subpopulations. Proinflammatory subpopulations such as Th1 and Th17 constitute a major source of proinflammatory cytokines that reduce endothelial integrity and stimulate astrocytes, resulting in the production of amyloid β. Anti-inflammatory subpopulations such as Th2 and Tregs reduce inflammation and regulate the function of Th1 and Th17. Recently, pathogenic Th17 has been shown to have a superior infiltrating capacity compared to other major CD4+ T cell subpopulations. Alzheimer's drugs such as donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne), and memantine (Namenda) are known to play an important part in regulating the mechanisms of the neurotransmitters. However, little is known about the effect of these drugs on CD4+ T cell subpopulations' infiltration of the brain during AD. In this review, we focus on understanding the influence of AD drugs on CD4+ T cell subpopulation interactions with the BBB in AD. While current AD therapies improve endothelial integrity and reduce astrocytes activations, they vary according to their influence on various CD4+ T cell subpopulations. Donepezil reduces the numbers of Th1 but not Th2, Rivastigmine inhibits Th1 and Th17 but not Th2, and memantine reduces Th1 but not Treg. However, none of the current AD drugs is specifically designed to target the dysregulated balance in the Th17/Treg axis. Future drug design approaches should specifically consider inhibiting CD4+ Th17 to improve AD prognosis.

Indexed as

Alzheimerblood brain barrierCD4+ T cellsmigrationTh17

Identifiers

PMID32948022
PMCPMC7558445
OpenAlexW3081413657

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.