Evidence map›Paper›PMID 36704003›Full record

ArticleFrontiers in neuroscience2022

Assessing the role of primary healthy microglia and gap junction blocker in hindering Alzheimer's disease neuroinflammatory type: Early approaches for therapeutic intervention.

Mai M Anwar, Esra Özkan, Narges Shomalizadeh, Selin Sapancı, Ceyda Özler, Judy Kesibi, Yasemin Gürsoy-Özdemir

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Mai M AnwarDepartment of Biochemistry, National Organization for Drug Control and Research/Egyptian Drug Authority, Cairo, Egypt.
Esra ÖzkanKoç University Research Center for Translational Medicine, KUTTAM, Koç University, Istanbul, Turkey.
Narges ShomalizadehKoç University Research Center for Translational Medicine, KUTTAM, Koç University, Istanbul, Turkey.
Selin SapancıKoç University Research Center for Translational Medicine, KUTTAM, Koç University, Istanbul, Turkey.
Ceyda ÖzlerKoç University Research Center for Translational Medicine, KUTTAM, Koç University, Istanbul, Turkey.
Judy KesibiKoç University Research Center for Translational Medicine, KUTTAM, Koç University, Istanbul, Turkey.
Yasemin Gürsoy-ÖzdemirKoç University Research Center for Translational Medicine, KUTTAM, Koç University, Istanbul, Turkey.
Koç University · TRNational Organization for Drug Control and Research · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a predominantly heterogeneous disease with a highly complex pathobiology. The presence of amyloid-beta (Aβ) depositions and the accumulation of hyperphosphorylated tau protein remain the characteristic hallmarks of AD. These hallmarks can be detected throughout the brain and other regions, including cerebrospinal fluid (CSF) and the spinal cord. Microglia cells, the brain-resident macrophage type of the brain, are implicated in maintaining healthy brain homeostasis. The localized administration of primary healthy microglia (PHM) is suggested to play a role in mitigating AD hallmark depositions and associated cognitive dysfunction. Carbenoxolone (CBX) is the most common gap junction blocker. It cannot effectively cross the blood-brain barrier (BBB) under systemic administration. Therefore, localized administration of CBX may be a recommended intervention against AD by acting as an antioxidant and anti-inflammatory agent. This study aims to determine whether the localized intracerebroventricular (ICV) administration of PHM and CBX may act as an effective therapeutic intervention for AD neuroinflammatory type. In addition, this study also aims to reveal whether detecting AD hallmarks in the spinal cord and CSF can be considered functional and effective during AD early diagnosis. Male albino rats were divided into four groups: control (group 1), lipopolysaccharide (LPS)-induced AD neuroinflammatory type (group 2), ICV injection of LPS + isolated PHM (group 3), and ICV injection of LPS + CBX (group 4). Morris water maze (MWM) was conducted to evaluate spatial working memory. The brain and spinal cord were isolated from each rat with the collection of CSF. Our findings demonstrate that the localized administration of PHM and CBX can act as promising therapeutic approaches against AD. Additionally, Aβ and tau toxic aggregates were detected in the spinal cord and the CSF of the induced AD model concomitant with the brain tissues. Overall, it is suggested that the ICV administration of PHM and CBX can restore normal brain functions and alleviate AD hallmark depositions. Detecting these depositions in the spinal cord and CSF may be considered in AD early diagnosis. As such, conducting clinical research is recommended to reveal the benefits of related therapeutic approaches compared with preclinical findings.

Indexed as

Alzheimer’s diseaseAβCBXhealthy microgliaICVinflammationmicrogliosistau protein

Identifiers

PMID36704003
PMCPMC9871931
OpenAlexW4315473078

What OpenQuestion holds

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LicenceCC BY
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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.