Mitochondrial Interaction with Serotonin in Neurobiology and Its Implication in Alzheimer’s Disease

Tian, Jing; Du, Eric; Guo, Lan

doi:10.3233/adr-230070

Cited by 3 publications

(1 citation statement)

References 165 publications

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“…In the dark, levels of dopamine are reduced in our body and are elevated during our light cycle of the day, as opposed to melatonin levels [16, 69, 70]. The increase we observed in the levels of both neurotransmitters might be due to elevated energy supply for synaptic activities, increased intracellular calcium levels, and light-induced neuronal activity [71, 72].…”

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

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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.

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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

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Biological Profile of Synthetic and Natural Indole Derivatives: Paving New Paths in Cancer Treatment

Janeiro,

Marques

2024

DDC

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The indole scaffold is considered a privileged framework in the design and synthesis of several active pharmaceutical ingredients, particularly as promising anticancer agents. Its presence in several bioactive natural compounds has caught the attention of the scientific community, which has been committed to unveiling its biosynthetic pathways and generating multiple derivatives with innovative synthetic routes. The large variety of structural derivatives enhances their use in multiple bioapplications and pharmacological activities. In this review, the reader will have easy access to some examples of natural and synthetic indole derivatives with antimicrobial, antidepressant, anti-inflammatory, antiviral, antimigraine, and antiemetic activity. However, the main topic of this review is related to cancer and the importance of indole derivatives as promising anticancer drugs. Two of the reasons why cancer is considered a massive problem worldwide are attributed to the struggle to develop target-specific drugs while avoiding drug resistance. Among countless drugs targeting specific proteins involved in tumorigenesis, prompting life quality in the treatment of several cancer types, protein kinases, desoxyribonucleic acid topoisomerases, and P-glycoprotein have been shown to be the main targets when it comes to the development of novel anticancer agents. Furthermore, indole and its derivatives are also studied regarding affinity to other targets related to cancer. This review aims to highlight the utility of the indole scaffold in anticancer drug design, inspiring the creation and synthesis of new derivatives that target specific proteins and address drug resistance challenges.

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Alzheimer’s Disease and Epilepsy: Exploring Shared Pathways and Promising Biomarkers for Future Treatments

Kalyvas,

Dimitriou,

Ioannidis

et al. 2024

JCM

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Background: Alzheimer’s disease (AD) and epilepsy represent two complex neurological disorders with distinct clinical manifestations, yet recent research has highlighted their intricate interplay. This review examines the association between AD and epilepsy, with particular emphasis on late-onset epilepsy of unknown etiology, increasingly acknowledged as a prodrome of AD. It delves into epidemiology, pathogenic mechanisms, clinical features, diagnostic characteristics, treatment strategies, and emerging biomarkers to provide a comprehensive understanding of this relationship. Methods: A comprehensive literature search was conducted, identifying 128 relevant articles published between 2018 and 2024. Results: Findings underscore a bidirectional relationship between AD and epilepsy, indicating shared pathogenic pathways that extend beyond traditional amyloid-beta and Tau protein pathology. These pathways encompass neuroinflammation, synaptic dysfunction, structural and network alterations, as well as molecular mechanisms. Notably, epileptic activity in AD patients may exacerbate cognitive decline, necessitating prompt detection and treatment. Novel biomarkers, such as subclinical epileptiform activity detected via advanced electroencephalographic techniques, offer promise for early diagnosis and targeted interventions. Furthermore, emerging therapeutic approaches targeting shared pathogenic mechanisms hold potential for disease modification in both AD and epilepsy. Conclusions: This review highlights the importance of understanding the relationship between AD and epilepsy, providing insights into future research directions. Clinical data and diagnostic methods are also reviewed, enabling clinicians to implement more effective treatment strategies.

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Mitochondrial Interaction with Serotonin in Neurobiology and Its Implication in Alzheimer’s Disease

Cited by 3 publications

References 165 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

Biological Profile of Synthetic and Natural Indole Derivatives: Paving New Paths in Cancer Treatment

Alzheimer’s Disease and Epilepsy: Exploring Shared Pathways and Promising Biomarkers for Future Treatments

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