Evidence map›Paper›PMID 28466999›Full record

ArticleCNS neuroscience & therapeutics2017

Sarsasapogenin-AA13 ameliorates Aβ-induced cognitive deficits via improving neuroglial capacity on Aβ clearance and antiinflammation.

Cui Huang, Dong Dong, Qian Jiao, Hui Pan, Lei Ma, Rui Wang

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 40 citations in OpenAlex.

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  5. Chronic cerebral hypoperfusion and blood-brain barrier disruption in uninjured brain areas of rhesus monkeys subjected to transient ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
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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

6 authors at 1 institution in 1 country.

Cui HuangShanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai, China.ORCID http://orcid.org/0000-0002-5725-9406
Dong DongShanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai, China.
Qian JiaoShanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai, China.
Hui PanShanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai, China.
Lei MaShanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai, China.
Rui WangShanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai, China.ORCID http://orcid.org/0000-0002-8753-8764
East China University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsSarsasapogenin has been reported to improve dementia symptoms somehow, probably through modulating the function of cholinergic system, suppressing neurofibrillary tangles, and inhibiting inflammation. However, the role of sarsasapogenin in response to beta-amyloid (Aβ) remains to be delineated. This study aimed to determine the therapeutic effect of sarsasapogenin-13 (AA13, a sarsasapogenin derivative) on learning and memory impairments in Aβ-injected mice, as well as the role of AA13 in neuroglia-mediated antiinflammation and Aβ clearance.

methodsFocusing on the role of AA13 in regulating glial responses to Aβ, we conducted behavioral, morphological, and protein expression studies to explore the effects of AA13 on Aβ clearance and inflammatory regulation.

resultsThe results indicated that oral administration of AA13 attenuated the memory deficits of intracerebroventricular (i.c.v.) Aβ-injected mice; also, AA13 protected neuroglial cells against Aβ-induced cytotoxicity. The further mechanical studies demonstrated that AA13 reversed the upregulation of proinflammatory M1 markers and increased the expression of antiinflammatory M2 markers in Aβ-treated cells. Furthermore, AA13 facilitated Aβ clearance through promoting Aβ phagocytosis and degradation. AA13 modulated the expression of fatty acid translocase (CD36), insulin-degrading enzyme (IDE), neprilysin (NEP), and endothelin-converting enzyme (ECE) in neuroglia.

conclusionThe present study indicated that the neuroprotective effect of AA13 might relate to its modulatory effects on microglia activation state, phagocytic ability, and expression of Aβ-degrading enzymes, which makes it a promising therapeutic agent in the early stage of Alzheimer's disease (AD).

Indexed as

Amyloid beta-PeptidesAnalysis of VarianceAnimalsAnimals, NewbornCells, CulturedCerebral CortexCognition DisordersDisease Models, AnimalDose-Response Relationship, DrugInjections, IntraventricularMaleMaze LearningMiceMice, Inbred ICRNeurogliaPeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide FragmentssarsasapogeninSpirostansantiinflammationbeta-amyloid clearanceneurogliaphagocytosissarsasapogenin-AA13

Identifiers

PMID28466999
PMCPMC6492744
OpenAlexW2610345393

What OpenQuestion holds

Textmetadata
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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.