Evidence map›Paper›PMID 36286468›Full record

ArticleMarine drugs2022

Astaxanthin Protection against Neuronal Excitotoxicity via Glutamate Receptor Inhibition and Improvement of Mitochondrial Function.

Swapna Kannothum Kandy, Madhura Milind Nimonkar, Suravi Sasmita Dash, Bhupesh Mehta, Yogananda S Markandeya

Open access · goldAbstract read
In one paragraph

Article in Marine drugs, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-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

22 citing papers in PubMed, 22 citations in OpenAlex.

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  18. Astaxanthin Inhibits HMarine drugs · 2024
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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 1 institution in 1 country.

Swapna Kannothum KandyDepartment of Biophysics, National Institute of Mental Health and Neuroscience (NIMHANS), Bengaluru 560029, India.
Madhura Milind NimonkarDepartment of Biophysics, National Institute of Mental Health and Neuroscience (NIMHANS), Bengaluru 560029, India.
Suravi Sasmita DashDepartment of Biophysics, National Institute of Mental Health and Neuroscience (NIMHANS), Bengaluru 560029, India.
Bhupesh MehtaDepartment of Biophysics, National Institute of Mental Health and Neuroscience (NIMHANS), Bengaluru 560029, India.
Yogananda S MarkandeyaDepartment of Biophysics, National Institute of Mental Health and Neuroscience (NIMHANS), Bengaluru 560029, India.ORCID 0000-0001-9783-2046
National Institute of Mental Health and Neurosciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excitotoxicity is known to associate with neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Amyotrophic lateral sclerosis and Huntington's disease, as well as aging, stroke, trauma, ischemia and epilepsy. Excessive release of glutamate, overactivation of glutamate receptors, calcium overload, mitochondrial dysfunction and excessive reactive oxygen species (ROS) formation are a few of the suggested key mechanisms. Astaxanthin (AST), a carotenoid, is known to act as an antioxidant and protect neurons from excitotoxic injuries. However, the exact molecular mechanism of AST neuroprotection is not clear. Thus, in this study, we investigated the role of AST in neuroprotection in excitotoxicity. We utilized primary cortical neuronal culture and live cell fluorescence imaging for the study. Our results suggest that AST prevents neuronal death, reduces ROS formation and decreases the abnormal mitochondrial membrane depolarization induced by excitotoxic glutamate insult. Additionally, AST modulates intracellular calcium levels by inhibiting peak and irreversible secondary sustained calcium levels in neurons. Furthermore, AST regulates the ionotropic glutamate subtype receptors NMDA, AMPA, KA and mitochondrial calcium. Moreover, AST decreases NMDA and AMPA receptor protein expression levels, while KA remains unaffected. Overall, our results indicate that AST protects neurons from excitotoxic neuronal injury by regulating ionotropic glutamate receptors, cytosolic secondary calcium rise and mitochondrial calcium buffering. Hence, AST could be a promising therapeutic agent against excitotoxic insults in neurodegenerative diseases.

Indexed as

Glutamic AcidNeurodegenerative Diseasesalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAntioxidantsCalciumHumansMitochondriaNeuronsN-MethylaspartateReactive Oxygen SpeciesReceptors, AMPAReceptors, GlutamateXanthophyllsalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAntioxidantsastaxanthineCalciumGlutamic AcidN-MethylaspartateReactive Oxygen SpeciesReceptors, AMPAReceptors, GlutamateXanthophyllsastaxanthincalciumcortical neuronsexcitotoxicitymitochondriareactive oxygen species

Identifiers

PMID36286468
PMCPMC9605357
OpenAlexW4306765914

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LicenceCC BY
Read underepoch 390

Registered trials

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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.