Metabolomic and transcriptomic profiles after immune stimulation in the zebrafish testes

Gelderen, T.A. van; Ladisa, Claudia; Salazar-Moscoso, M.; Folgado, C.; Habibi, Hamid R.; Ribas, Laia

doi:10.1016/j.ygeno.2023.110581

Cited by 4 publications

(2 citation statements)

References 109 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Three pathways were shared by metabolomics studies of serum samples from diabetic patients: 1) alanine, aspartate, and glutamate metabolism, 2) glycine, serine, and threonine metabolism, and 3) valine, leucine, and isoleucine biosynthesis [98]. Transcriptomic and metabolomic joint analysis after an immune challenge with LPS in Zebra fish, revealed enrichment of alanine, aspartate, and glutamate metabolism and aminoacyl-tRNA biosynthesis [99]. They reported Krebs cycle was one of the most affected cycles in the mitochondria and highlighted in both studies when analysis was performed by the KEGG pathway [98, 99].…”

Section: Discussionmentioning

confidence: 99%

“…Transcriptomic and metabolomic joint analysis after an immune challenge with LPS in Zebra fish, revealed enrichment of alanine, aspartate, and glutamate metabolism and aminoacyl-tRNA biosynthesis [99]. They reported Krebs cycle was one of the most affected cycles in the mitochondria and highlighted in both studies when analysis was performed by the KEGG pathway [98, 99].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The 40 Hz flickering light restores synaptic plasticity and mitochondrial phenotype in experimental model of Alzheimer’s disease

Barzegar behrooz,

Aghanoori,

Khodagholi

et al. 2024

Preprint

View full text Add to dashboard Cite

Alzheimer's disease (AD) is the most prevalent form of dementia and a public health priority. The causes of AD are not completely understood. Pathogenetic factors including mitochondrial dysfunction, oxidative stress, reduced energy status, and compromised ion channels contribute to the onset and progression of the disease. Flickering light therapy in experimental and clinical AD has shown promising outcomes. However, the mechanisms behind the effect of flickering light at the molecular and cellular level has not yet been fully investigated. In this study, we established streptozotocin (STZ)-induced AD models by intracerebroventricular (ICV) injection of STZ in Wistar rats and monitored their memory decline. Sham and AD rats were either exposed or not exposed to 40 Hz flickering light for 7 consecutive days after 7 days of STZ injection. Memory and cognition-related behavioral analysis, pathological, electrophysiological, and biochemical assessment of the brain tissue, and mitochondrial function assays were conducted after the treatment. Cognitive and memory impairment, examined by Morris water maze (MWM), novel object recognition (NOR), and passive avoidance (PA) test, was observed in the STZ-induced AD rats and light treatment improved these behaviors. STZ injection led to significant accumulation of reactive oxygen species (ROS) and amyloid beta (Aβ), decreased serotonin and dopamine levels, and mitochondrial respiration. The 40 Hz flickering light reversed all these parameters in the light treatment group. The synaptic plasticity of STZ-induced AD rats was severely affected, but flickering light prevented the loss of synaptic plasticity and activity in the light-treated AD rats. Additionally, flickering 40 Hz white light elevated the levels of mitochondrial metabolites and the current and possible opening of the mitochondrial calcium-sensitive potassium (mitoBKCa) channel which were significantly downregulated in AD rat neurons. The 40 Hz flickering light restored mitochondrial function and synaptic plasticity of AD rat neurons and improved the cognition of animals; therefore, it can be a promising strategy to reduce AD progression.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The 40 Hz flickering light restores synaptic plasticity and mitochondrial phenotype in experimental model of Alzheimer’s disease

Barzegar behrooz,

Aghanoori,

Khodagholi

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

Integration analysis of transcriptome and metabolome revealed the potential mechanism of spermatogenesis in Tibetan sheep (Ovis aries) at extreme high altitude

Zhang,

An,

Yuan

et al. 2024

Genomics

View full text Add to dashboard Cite

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

Barzegar Behrooz,

Aghanoori,

Nazari

et al. 2024

Sci Rep

View full text Add to dashboard Cite

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. Supplementary Information The online version contains supplementary material available at 10.1038/s41598-024-78528-7.

show abstract

Metabolomic and transcriptomic profiles after immune stimulation in the zebrafish testes

Cited by 4 publications

References 109 publications

The 40 Hz flickering light restores synaptic plasticity and mitochondrial phenotype in experimental model of Alzheimer’s disease

The 40 Hz flickering light restores synaptic plasticity and mitochondrial phenotype in experimental model of Alzheimer’s disease

Integration analysis of transcriptome and metabolome revealed the potential mechanism of spermatogenesis in Tibetan sheep (Ovis aries) at extreme high altitude

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

Contact Info

Product

Resources

About