scholarly journals Are Circadian Disturbances a Core Pathophysiological Component of Schizophrenia?

2020 ◽  
Vol 35 (4) ◽  
pp. 325-339
Author(s):  
Tara C. Delorme ◽  
Lalit K. Srivastava ◽  
Nicolas Cermakian

Schizophrenia is a multifactorial disorder caused by a combination of genetic variations and exposure to environmental insults. Sleep and circadian rhythm disturbances are a prominent and ubiquitous feature of many psychiatric disorders, including schizophrenia. There is growing interest in uncovering the mechanistic link between schizophrenia and circadian rhythms, which may directly affect disorder outcomes. In this review, we explore the interaction between schizophrenia and circadian rhythms from 2 complementary angles. First, we review evidence that sleep and circadian rhythm disturbances constitute a fundamental component of schizophrenia, as supported by both human studies and animal models with genetic mutations related to schizophrenia. Second, we discuss the idea that circadian rhythm disruption interacts with existing risk factors for schizophrenia to promote schizophrenia-relevant behavioral and neurobiological abnormalities. Understanding the mechanistic link between schizophrenia and circadian rhythms will have implications for mitigating risk to the disorder and informing the development of circadian-based therapies.

Biomolecules ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1186
Author(s):  
Silvia Sgambellone ◽  
Laura Lucarini ◽  
Cecilia Lanzi ◽  
Emanuela Masini

Glaucoma is a multifactorial neuropathy characterized by increased intraocular pressure (IOP), and it is the second leading cause of blindness worldwide after cataracts. Glaucoma combines a group of optic neuropathies characterized by the progressive degeneration of retinal ganglionic cells (RGCs). Increased IOP and short-term IOP fluctuation are two of the most critical risk factors in glaucoma progression. Histamine is a well-characterized neuromodulator that follows a circadian rhythm, regulates IOP and modulates retinal circuits and vision. This review summarizes findings from animal models on the role of histamine and its receptors in the eye, focusing on the effects of histamine H3 receptor antagonists for the future treatment of glaucomatous patients.


2018 ◽  
Vol 24 (22) ◽  
pp. 2549-2555 ◽  
Author(s):  
Senthil Kumaran Satyanarayanan ◽  
Huanxing Su ◽  
Yi-Wen Lin ◽  
Kuan-Pin Su

Background: Circadian rhythm disruption underlies the pathophysiology of psychiatric disorders, especially depression. Both pharmacological and non-pharmacological strategies affecting endogenous circadian rhythms have been developed with specificity to alter the circadian dysfunction. The current management strategy with antidepressants is far from being satisfactory in addressing this issue. In recent years, attempts at discovering new antidepressants focused on a melatonergic system which is known to be altered in depression have led to a potential option for treatment of depression. Methods: We reviewed all recently published relevant articles on melatonin and its analogues to look for their implication in the treatment of circadian rhythm disruption and depression. Results: Melatonin, a pleiotropic regulator molecule and its analogues (ramelteon, agomelatine, TIK-301, Neu- P11 and tasimelteon) have been observed to resynchronize the circadian rhythm and some were said to alleviate depressive symptoms in depressed subjects. Conclusion: This review focuses on substantial advances in the melatonin-based chronobiologic intervention and its responses in the treatment of depression.


2016 ◽  
Vol 310 (6) ◽  
pp. F454-F455 ◽  
Author(s):  
Michelle L. Gumz

Do your kidneys know what time it is? Mounting evidence from human studies and animal models strongly suggests that the answer to this question is yes. The time has come to start reporting the time of day at which renal physiology studies are performed.


2021 ◽  
pp. 1-7
Author(s):  
Andrew D. Grotzinger

Abstract Psychiatric disorders overlap substantially at the genetic level, with family-based methods long pointing toward transdiagnostic risk pathways. Psychiatric genomics has progressed rapidly in the last decade, shedding light on the biological makeup of cross-disorder risk at multiple levels of analysis. Over a hundred genetic variants have been identified that affect multiple disorders, with many more to be uncovered as sample sizes continue to grow. Cross-disorder mechanistic studies build on these findings to cluster transdiagnostic variants into meaningful categories, including in what tissues or when in development these variants are expressed. At the upper-most level, methods have been developed to estimate the overall shared genetic signal across pairs of traits (i.e. single-nucleotide polymorphism-based genetic correlations) and subsequently model these relationships to identify overarching, genomic risk factors. These factors can subsequently be associated with external traits (e.g. functional imaging phenotypes) to begin to understand the makeup of these transdiagnostic risk factors. As psychiatric genomic efforts continue to expand, we can begin to gain even greater insight by including more fine-grained phenotypes (i.e. symptom-level data) and explicitly considering the environment. The culmination of these efforts will help to inform bottom-up revisions of our current nosology.


Cancers ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1700
Author(s):  
Melissa Chalada ◽  
Charmaine A. Ramlogan-Steel ◽  
Bijay P. Dhungel ◽  
Christopher J. Layton ◽  
Jason C. Steel

Uveal melanoma (UM) is currently classified by the World Health Organisation as a melanoma caused by risk factors other than cumulative solar damage. However, factors relating to ultraviolet radiation (UVR) susceptibility such as light-coloured skin and eyes, propensity to burn, and proximity to the equator, frequently correlate with higher risk of UM. These risk factors echo those of the far more common cutaneous melanoma (CM), which is widely accepted to be caused by excessive UVR exposure, suggesting a role of UVR in the development and progression of a proportion of UM. Indeed, this could mean that countries, such as Australia, with high UVR exposure and the highest incidences of CM would represent a similarly high incidence of UM if UVR exposure is truly involved. Most cases of UM lack the typical genetic mutations that are related to UVR damage, although recent evidence in a small minority of cases has shown otherwise. This review therefore reassesses statistical, environmental, anatomical, and physiological evidence for and against the role of UVR in the aetiology of UM.


Author(s):  
Peter H. Rudebeck ◽  
Alicia Izquierdo

AbstractEfficient foraging is essential to survival and depends on frontal cortex in mammals. Because of its role in psychiatric disorders, frontal cortex and its contributions to reward procurement have been studied extensively in both rodents and non-human primates. How frontal cortex of these animal models compares is a source of intense debate. Here we argue that translating findings from rodents to non-human primates requires an appreciation of both the niche in which each animal forages as well as the similarities in frontal cortex anatomy and function. Consequently, we highlight similarities and differences in behavior and anatomy, before focusing on points of convergence in how parts of frontal cortex contribute to distinct aspects of foraging in rats and macaques, more specifically. In doing so, our aim is to emphasize where translation of frontal cortex function between species is clearer, where there is divergence, and where future work should focus. We finish by highlighting aspects of foraging for which have received less attention but we believe are critical to uncovering how frontal cortex promotes survival in each species.


2021 ◽  
Vol 36 (4) ◽  
pp. 523-543
Author(s):  
Vanessa Trindade Bortoluzzi ◽  
Carlos Severo Dutra Filho ◽  
Clovis Milton Duval Wannmacher

Author(s):  
Takashi Hosono ◽  
Masanori Ono ◽  
Takiko Daikoku ◽  
Michihiro Mieda ◽  
Satoshi Nomura ◽  
...  

Abstract Background Skipping breakfast is associated with dysmenorrhea in young women. This suggests that the delay of food intake in the active phase impairs uterine functions by interfering with circadian rhythms. Objective To examine the relationship between the delay of feeding and uterine circadian rhythms, we investigated the effects of the first meal occasion in the active phase on the uterine clock. Methods Zeitgeber time (ZT) was defined as ZT 0 (8:45) with lights on and ZT 12 (20:45) with lights off. Young female mice (8 weeks of age) were divided into 3 groups: group I (ad-libitum feeding), group II (time-restricted feeding during ZT12–16, initial 4 hours of the active period), and group III (time-restricted feeding during ZT20–24, last 4 hours of the active period, a breakfast-skipping model). After two weeks of dietary restriction, mice in each group were sacrificed at 4-hour intervals and the expression profiles of uterine clock genes, Bmal1, Per1, Per2, and Cry1, were examined. Results qPCR and Western blot analyses demonstrated synchronized circadian clock gene expression within the uterus. Immunohistochemical analysis confirmed that Bmal1 protein expression was synchronized among the endometrium and myometrium. In groups I and II, mRNA expression of Bmal1 was elevated after ZT12 at the start of the active phase. In contrast, Bmal1 expression was elevated just after ZT20 in group III, showing that the uterine clock rhythm had shifted 8 hours backward. The changes in Bmal1 protein expression were confirmed by Western blot analysis. Conclusion This study is the first to indicate that time-restricted feeding regulates a circadian rhythm of the uterine clock that is synchronized throughout the uterine body. These findings suggest that the uterine clock system is a new candidate to explain the etiology of breakfast skipping-induced uterine dysfunction.


2021 ◽  
Vol 22 (2) ◽  
pp. 676
Author(s):  
Andy W. C. Man ◽  
Huige Li ◽  
Ning Xia

Every organism has an intrinsic biological rhythm that orchestrates biological processes in adjusting to daily environmental changes. Circadian rhythms are maintained by networks of molecular clocks throughout the core and peripheral tissues, including immune cells, blood vessels, and perivascular adipose tissues. Recent findings have suggested strong correlations between the circadian clock and cardiovascular diseases. Desynchronization between the circadian rhythm and body metabolism contributes to the development of cardiovascular diseases including arteriosclerosis and thrombosis. Circadian rhythms are involved in controlling inflammatory processes and metabolisms, which can influence the pathology of arteriosclerosis and thrombosis. Circadian clock genes are critical in maintaining the robust relationship between diurnal variation and the cardiovascular system. The circadian machinery in the vascular system may be a novel therapeutic target for the prevention and treatment of cardiovascular diseases. The research on circadian rhythms in cardiovascular diseases is still progressing. In this review, we briefly summarize recent studies on circadian rhythms and cardiovascular homeostasis, focusing on the circadian control of inflammatory processes and metabolisms. Based on the recent findings, we discuss the potential target molecules for future therapeutic strategies against cardiovascular diseases by targeting the circadian clock.


2006 ◽  
Vol 40 (4) ◽  
pp. 355-361 ◽  
Author(s):  
Hung-Chi Wu ◽  
Pesus Chou ◽  
Frank Huang-Chih Chou ◽  
Chao-Yueh Su ◽  
Kuan-Yi Tsai ◽  
...  

Objective: To investigate quality of life (QOL) and related risk factors in Taiwanese earthquake survivors diagnosed with different psychiatric disorders 3 years after the 1999 Chi-Chi earthquake. Method: This study was a population survey. Trained assistants used the Medical Outcomes Study Short Form-36 (MOS SF-36) and questionnaires to interview 405 respondents (189 men and 216 women) aged 16 years or older, who had been exposed to the earthquake. Psychiatrists interviewed the same respondents using the Mini-International Neuropsychiatric Interview, with an adjusted response rate of 70.2%. Results: The prevalence range for psychiatric disorders in the earthquake survivors was 0.2–7.2% 3 years after the Chi-Chi earthquake, with rates for major depression (MD) and posttraumatic stress disorder (PTSD) of 6.4% and 4.4%, respectively. The QOL scores for the PTSD/MD group were lower than for the other two diagnostic groups, as determined by assessment of physical and mental aspects of functional integrity from MOS SF-36 scores. The predictors for poor QOL were age, female gender, economic problems, physical illness, subjective assessment of memory and social-activity decline and diagnosis of PTSD or MD. Conclusion: The QOL for earthquake survivors with psychiatric disorders, especially PTSD or MD, was inferior compared with the mentally healthy analogues, with contemporaneous decreases in mental and physical function scores across the QOL subscales. The persistence of long-term economic problems was one of many important factors affecting QOL.


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