Evidence map›Paper›PMID 36012296›Full record

ArticleInternational journal of molecular sciences2022

Microglia Impairs Proliferation and Induces Senescence In-Vitro in NGF Releasing Cells Used in Encapsulated Cell Biodelivery for Alzheimer's Disease Therapy.

Sumonto Mitra, Ruchi Gera, Julia Sundheimer, Marine Lemee, Lars U Wahlberg, Bengt Linderoth, Maria Eriksdotter, Homira Behbahani

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
  3. Advancements in investigating the role of cerebral small vein loss in Alzheimer's disease-related pathological changes.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Review
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

8 authors at 3 institutions in 2 countries.

Sumonto MitraDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of NVS, Karolinska Institutet, 141 52 Huddinge, Sweden.ORCID 0000-0001-6381-5344
Ruchi GeraDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of NVS, Karolinska Institutet, 141 52 Huddinge, Sweden.
Julia SundheimerDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of NVS, Karolinska Institutet, 141 52 Huddinge, Sweden.
Marine LemeeDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of NVS, Karolinska Institutet, 141 52 Huddinge, Sweden.
Lars U WahlbergGloriana Therapeutics, Inc., Providence, RI 02885, USA.
Bengt LinderothDepartment of Clinical Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden.
Maria EriksdotterDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of NVS, Karolinska Institutet, 141 52 Huddinge, Sweden.
Homira BehbahaniDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of NVS, Karolinska Institutet, 141 52 Huddinge, Sweden.
Karolinska Institutet · SEKarolinska University Hospital · SEProvidence College · US

Funding

Gamla Tjänarinnor stiftelse 2019-00846Gun and Bertil Stohne's Foundation 20200917Hjärnfonden FO2020-0228Swedish Research Council 2020-02014
6 · The paper itself

Abstract

There is no cure yet available for Alzheimer's disease (AD). We recently optimized encapsulated cell biodelivery (ECB) devices releasing human mature nerve growth factor (hmNGF), termed ECB-NGF, to the basal forebrain of AD patients. The ECB-NGF delivery resulted in increased CSF cholinergic markers, improved glucose metabolism, and positive effects on cognition in AD patients. However, some ECB-NGF implants showed altered hmNGF release post-explantation. To optimize the ECB-NGF platform for future therapeutic purposes, we initiated in-vitro optimization studies by exposing ECB-NGF devices to physiological factors present within the AD brain. We report here that microglia cells can impair hmNGF release from ECB-NGF devices in-vitro, which can be reversed by transferring the devices to fresh culture medium. Further, we exposed the hmNGF secreting human ARPE-19 cell line (NGC0211) to microglia (HMC3) conditioned medium (MCM; untreated or treated with IL-1β/IFNγ/Aβ

Indexed as

Alzheimer DiseaseBasal ForebrainAmyloid beta-PeptidesBiomarkersCell ProliferationHumansMicrogliaNerve Growth FactorAmyloid beta-PeptidesBiomarkersNerve Growth FactorAlzheimer’s disease (AD)amyloid beta (Aβ)drug deliveryencapsulated cell biodelivery (ECB)inflammationmicroglianerve growth factor (NGF)senescencetherapy

Identifiers

PMID36012296
PMCPMC9409429
OpenAlexW4291885317

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.