Browsing by Subject "Circadian rhythm"

Now showing 1 - 4 of 4

Open Access
Color-enrichment semiconductor nanocrystals for biorhythm-friendly backlighting
(De Gruyter, 2018) Erdem, T.; Demir, Hilmi Volkan
Nanocrystals (NCs) offer great opportunities for developing novel light-emitting devices possessing superior properties such as high quality indoor lighting, efficient outdoor lighting, and display backlighting with increased color definition. The narrow-band emission spectra of these materials also offer opportunities to protect the human daily biological rhythm against the adverse effects of display backlighting. For this purpose, here we address this problem using color converting NCs and analyzed the effect of the NC integrated color converting light-emitting diode (NC LED) backlight spectra on the human circadian rhythm. We employed the three existing models including the circadian light, the melanopic sensitivity function, and the circadian effect factor by simultaneously satisfying the National Television Standards Committee (NTSC) requirements. The results show that NC LED backlighting exhibits (i) 33% less disruption on the circadian cycle if the same color gamut of the commercially available YAG:Ce LED is targeted and (ii) 34% wider color gamut while causing 4.1% weaker disruption on the circadian rhythm compared to YAG:Ce LED backlight if the NTSC color gamut is fully reproduced. Furthermore, we found out that blue and green emission peaks have to be located at 465 with 30 nm bandwidth and at 535 nm with 20 nm bandwidth, respectively, for a circadian rhythm friendly design while the red component offers flexibility around the peak emission wavelength at 636 nm as opposed to the requirements of quality indoor lighting. These design considerations introduced as a new design perspective for the displays of future will help avoiding the disruption of the human circadian rhythm.
Open Access
Longevity and circadian rhythm in Caenorhabditis elegans: the impact of lithium chloride
(2024-06) Temirci, Elif Sena
Lithium chloride (LiCl) is a popular treatment for various neurological disorders, especially bipolar disorders. While its complete mechanism of action remains partially elucidated, LiCl has been found to support new memory formation by triggering the construction of new neurons, reducing senescence, and regulating the circadian rhythm, particularly in bipolar patients, where it counteracts their abnormally fast biological clock. The circadian rhythm is vital in determining efficiency, understanding energy consumption, and biochemical balance for all organisms. This rhythm includes regulating body functions by the day/night cycle. Caenorhabditis elegans (C. elegans) is one of the most robust organisms for modeling circadian rhythm, although it lives in the soil. Therefore, by employing C. elegans as a model system, valuable insights could be gained for these complex processes. This study aims to elucidate the complex relationship between LiCl, circadian rhythms, and longevity, as disruptions in these pathways are implicated in neurodegenerative diseases and age-related cognitive and motor decline. In this project, white light was employed to manipulate the circadian rhythm in C. elegans, with one group additionally receiving LiCl treatment in addition to light exposure. The study focused on longevity, response to environmental factors, and circadian rhythm. To elucidate the effect on longevity, lifespan measurements showed that LiCl treatment extended the lifespan of C. elegans under both light and dark conditions, with a shorter lifespan observed in the light. Additionally, when comparing the effect of specific developmental time points, the signs of aging appeared later in the dark compared to the light. The differential gene expression of longevity genes suggested that LiCl treatment could impact gene expression, particularly the age-1 gene, but not the daf-16 gene. Furthermore, the response to environmental changes was examined imilarly and it was observed that C. elegans responded to the circadian rhythm disruption caused by light and LiCl administration. In conclusion, this study suggests that LiCl treatment has the potential to mitigate the adverse effects of circadian rhythm disruptions and reverse the aging process of C. elegans.
Open Access
Mutation of the human circadian clock gene CRY1 in familial delayed sleep phase disorder
(Cell Press, 2017) Patke, A.; Murphy, P. J.; Onat, O. E.; Krieger, A. C.; Özçelik, T.; Campbell, S. S.; Young, M. W.
Patterns of daily human activity are controlled by an intrinsic circadian clock that promotes ∼24 hr rhythms in many behavioral and physiological processes. This system is altered in delayed sleep phase disorder (DSPD), a common form of insomnia in which sleep episodes are shifted to later times misaligned with the societal norm. Here, we report a hereditary form of DSPD associated with a dominant coding variation in the core circadian clock gene CRY1, which creates a transcriptional inhibitor with enhanced affinity for circadian activator proteins Clock and Bmal1. This gain-of-function CRY1 variant causes reduced expression of key transcriptional targets and lengthens the period of circadian molecular rhythms, providing a mechanistic link to DSPD symptoms. The allele has a frequency of up to 0.6%, and reverse phenotyping of unrelated families corroborates late and/or fragmented sleep patterns in carriers, suggesting that it affects sleep behavior in a sizeable portion of the human population. © 2017 Elsevier Inc.
Open Access
Using zebrafish disease model in molecular research on neurodevelopmental disorder generation
(2025-01) Başcı, Ayşe Reyyan Kutan
In this thesis, zebrafish were used as a model organism to study two different projects: issues stemming from the dopaminergic system during the neurodevelopmental period, specifically ADHD, and a Parkinson’s disease model representing dopaminergic system disorders in old age. This approach allowed for an investigation of the lifelong effects of disorders caused by dopaminergic system dysfunction. Attention-deficit/hyperactivity disorder (ADHD) is a prevalent condition characterized by persistent inattention, hyperactivity, and impulsivity, often leading to significant impairments in daily functioning. Numerous medications have been developed to manage ADHD, with methylphenidate (commonly known as Ritalin or Concerta) being the most widely used active compound. While methylphenidate effectively improves attention, focus, and emotional regulation, its long-term use can lead to behavioral issues such as increased depression and anxiety, as well as physical side effects like sleep disturbances and decreased sensitivity to rewards. These side effects are more challenging to compensate for in adults compared to children, which may leave permanent effects. This study aims to investigate the long-term effects of methylphenidate use in adult women, with a focus on its role in sleep disorders, circadian rhythm disruption, and the potential implications for pregnancy, specifically on the susceptibility of offspring to accelerated brain aging. Our hypothesis is that methylphenidate use during pregnancy may contribute to changes in offspring telomere length and gene methylation patterns associated with brain aging, thereby increasing their vulnerability to neurodegeneration. To evaluate this, telomere length and methylation analyses were conducted on genes linked to brain aging in second-generation offspring. Additionally, our hypothesis is that therapeutic interventions, such as melatonin for regulating sleep disturbances and oxytocin as an alternative to mitigate methylphenidate’s side effects, may have protective effects. Zebrafish were used as the model organism in this study due to their high genetic similarity to humans and their ease of egg production, enabling multi-generational studies. As a result of this study, it was determined that neuroinflammation caused by circadian rhythm disruption and maternal stress was reduced through melatonin & methylphenidate and oxytocin & methylphenidate combinational treatments. In the offspring of the next generation, it was observed that the telomere length inherited at birth was shorter when treated with methylphenidate only. In the second research project of this thesis, the origins of Parkinson’s disease from two distinct locations—the brain and the gut—were investigated. Parkin-son’s disease is a neurodegenerative disorder characterized by the loss or reduction of dopaminergic neurons in the central nervous system. It is associated with aggregation of alpha-synuclein fibrils and resulting in motor function impairments. In the previous phase of this research, transgenic zebrafish models of Parkinson’s disease were developed by integrating human alpha-synuclein gene into the zebrafish genome at the single-cell stage. In this phase of thesis, six-month-old transgenic zebrafish were used to test the hypothesis that Parkinson’s disease can originate from either the brain or the gut. Alpha-synuclein protein was injected into the brain and gut, and its migration between these two organs was analyzed. The migration of alpha-synuclein fibrils was validated using immuno-histochemistry techniques. Behavioral changes and motor function impairments were assessed using novel tank tests, swim endurance tests, and hyposmia tests. As a result of the study, it was validated that alpha-synuclein fibrils injected into the brain-to-gut and gut-to-brain migrate at different speeds.