Evidence map›Paper›PMID 24203394›Full record

ArticleNeuromolecular medicine2014

Monitoring of neuronal loss in the hippocampus of Aβ-injected rat: autophagy, mitophagy, and mitochondrial biogenesis stand against apoptosis.

Fatemeh Shaerzadeh, Fereshteh Motamedi, Dariush Minai-Tehrani, Fariba Khodagholi

Abstract read
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In one paragraph

Article in Neuromolecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 49 citations in OpenAlex.

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  8. Age-Related Increase of Insulin-Degrading Enzyme Is Inversely Correlated with Cognitive Function in APPswe/PS1dE9 Mice.Medical science monitor : international medical journal of experimental and clinical research · 2018
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  11. The Temporal Pattern, Flux, and Function of Autophagy in Spinal Cord Injury.International journal of molecular sciences · 2017
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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

4 authors at 2 institutions in 1 country.

Fatemeh ShaerzadehNeuroBiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Fereshteh Motamedi
Dariush Minai-Tehrani
Fariba Khodagholi
Shahid Beheshti University of Medical Sciences · IRShahid Beheshti University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the present study, we tried to answer the following questions: which kind of defense pathways are activated after Aβ insult? How defense systems react against noxious effects of Aβ and whether they are able to deal against apoptosis or not? So, we traced some molecular pathways including autophagy, mitophagy, and mitochondrial biogenesis before reaching to the endpoint of apoptosis. Besides, we measured the function of mitochondria after injection of Aβ (1-42) in CA1 area of hippocampus as a model of Alzheimer's disease (AD). Based on our data, autophagy markers reached to their maximum level and returned to the control level as apoptotic markers started to increase. As a specialized form of autophagy, mitophagy markers followed the trend of autophagy markers. Whereas mitochondrial dynamic processes shifted toward fission, mitochondrial biogenesis was severely affected by Aβ and significantly decreased. Alongside suppression of mitochondrial biogenesis, activity of specific enzymes involved in antioxidant defense system, electron transport chain, and tricarboxylic acid cycle (TCA) decreased in response to the Aβ. Activity of antioxidant enzymes increased at first and then decreased significantly compared to the control. TCA enzymes aconitase and malate dehydrogenase activities reduced immediately while citrate synthase and fumarase activities did not change. Based on our finding, monitoring of the master molecules of intracellular cascades and determining their trends before the destructive function of Aβ could be the target of therapeutic issues for AD.

Indexed as

Aconitate HydrataseAmyloid beta-PeptidesAnimalsApoptosisAutophagyCA1 Region, HippocampalCatalaseCitrate (si)-SynthaseCitric Acid CycleCytochromesElectron TransportEnzyme InductionFumarate HydrataseGlutathioneMalate DehydrogenaseMaleAconitate HydrataseAmyloid beta-Peptidesamyloid beta-protein (1-42)CatalaseCitrate (si)-SynthaseCytochromesFumarate HydrataseGlutathioneMalate DehydrogenaseNerve Tissue ProteinsPeptide FragmentsProtein KinasesPTEN-Induced Putative KinaseReactive Oxygen SpeciesSuperoxide Dismutase

Identifiers

PMID24203394
OpenAlexW2012960319

What OpenQuestion holds

Textmetadata
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.