Evidence map›Paper›PMID 39506052›Full record

ArticleScientific reports2024

40 Hz light preserves synaptic plasticity and mitochondrial function in Alzheimer's disease model.

Amir Barzegar Behrooz, Mohamad-Reza Aghanoori, Maryam Nazari, Hamid Latifi-Navid, Fatemeh Vosoughian, Mojdeh Anjomani, Jabar Lotfi, Abolhassan Ahmadiani, Afsaneh Eliassi, Fatemeh Nabavizadeh and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

14 authors.

Amir Barzegar BehroozNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohamad-Reza AghanooriNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Maryam NazariNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Hamid Latifi-NavidElectrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Fatemeh VosoughianNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mojdeh AnjomaniNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Jabar LotfiDepartment of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Abolhassan AhmadianiNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Afsaneh EliassiNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Fatemeh NabavizadehElectrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Elham SoleimaniNeuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Saeid Ghavami *Faculty of Medicine in Zabrze, University of Technology in Katowice, Zabrze, 41-800, Poland.
Fariba Khodagholi *Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Javad Fahanik-Babaei *Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. Fahanikbabaei1358@gmail.com.ORCID 0000-0001-6707-132X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most prevalent type of dementia. Its causes are not fully understood, but it is now known that factors like mitochondrial dysfunction, oxidative stress, and compromised ion channels contribute to its onset and progression. Flickering light therapy has shown promise in AD treatment, though its mechanisms remain unclear. In this study, we used a rat model of streptozotocin (STZ)-induced AD to evaluate the effects of 40 Hz flickering light therapy. Rats received intracerebroventricular (ICV) STZ injections, and 7 days after, they were exposed to 40 Hz flickering light for 15 min daily over seven days. Cognitive and memory functions were assessed using Morris water maze, novel object recognition, and passive avoidance tests. STZ-induced AD rats exhibited cognitive decline, elevated reactive oxygen species, amyloid beta accumulation, decreased serotonin and dopamine levels, and impaired mitochondrial function. However, light therapy prevented these effects, preserving cognitive function and synaptic plasticity. Additionally, flickering light restored mitochondrial metabolites and normalized ATP-insensitive mitochondrial calcium-sensitive potassium (mitoBKCa) channel activity, which was otherwise downregulated in AD rats. Our findings suggest that 40 Hz flickering light therapy could be a promising treatment for neurodegenerative disorders like AD by preserving synaptic and mitochondrial function.

Indexed as

Alzheimer DiseaseDisease Models, AnimalMitochondriaNeuronal PlasticityAmyloid beta-PeptidesAnimalsLightMaleOxidative StressPhototherapyRatsReactive Oxygen SpeciesStreptozocinAmyloid beta-PeptidesReactive Oxygen SpeciesStreptozocinAlzheimer’s diseaseFlickering 40 Hz white lightLTPMitoBKCa+2Mitochondrial functionMitochondrial metabolitesSynaptic plasticity

Identifiers

PMID39506052
PMCPMC11541745

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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.