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Translational Neurodegeneration Feb 2023Disruptions of circadian rhythms and sleep cycles are common among neurodegenerative diseases and can occur at multiple levels. Accumulating evidence reveals a... (Review)
Review
Disruptions of circadian rhythms and sleep cycles are common among neurodegenerative diseases and can occur at multiple levels. Accumulating evidence reveals a bidirectional relationship between disruptions of circadian rhythms and sleep cycles and neurodegenerative diseases. Circadian disruption and sleep disorders aggravate neurodegeneration and neurodegenerative diseases can in turn disrupt circadian rhythms and sleep. Importantly, circadian disruption and various sleep disorders can increase the risk of neurodegenerative diseases. Thus, harnessing the circadian biology findings from preclinical and translational research in neurodegenerative diseases is of importance for reducing risk of neurodegeneration and improving symptoms and quality of life of individuals with neurodegenerative disorders via approaches that normalize circadian in the context of precision medicine. In this review, we discuss the implications of circadian disruption and sleep disorders in neurodegenerative diseases by summarizing evidence from both human and animal studies, focusing on the bidirectional links of sleep and circadian rhythms with prevalent forms of neurodegeneration. These findings provide valuable insights into the pathogenesis of neurodegenerative diseases and suggest a promising role of circadian-based interventions.
Topics: Animals; Humans; Quality of Life; Sleep; Circadian Rhythm; Neurodegenerative Diseases; Sleep Wake Disorders
PubMed: 36782262
DOI: 10.1186/s40035-023-00340-6 -
International Journal of Molecular... Mar 2023Endocrine-disrupting chemicals (EDCs) have significant impacts on biological systems, and have been shown to interfere with physiological systems, especially by... (Review)
Review
Endocrine-disrupting chemicals (EDCs) have significant impacts on biological systems, and have been shown to interfere with physiological systems, especially by disrupting the hormone balance. During the last few decades, EDCs have been shown to affect reproductive, neurological, and metabolic development and function and even stimulate tumor growth. EDC exposure during development can disrupt normal development patterns and alter susceptibility to disease. Many chemicals have endocrine-disrupting properties, including bisphenol A, organochlorines, polybrominated flame retardants, alkylphenols, and phthalates. These compounds have gradually been elucidated as risk factors for many diseases, such as reproductive, neural, and metabolic diseases and cancers. Endocrine disruption has been spread to wildlife and species that are connected to the food chains. Dietary uptake represents an important source of EDC exposure. Although EDCs represent a significant public health concern, the relationship and specific mechanism between EDCs and diseases remain unclear. This review focuses on the disease-EDC relationship and the disease endpoints associated with endocrine disruption for a better understanding of the relationship between EDCs-disease and elucidates the development of new prevention/treatment opportunities and screening methods.
Topics: Animals; Endocrine Disruptors; Reproduction; Animals, Wild; Endocrine System; Nervous System
PubMed: 36982431
DOI: 10.3390/ijms24065342 -
Neuron Apr 2012Exome sequencing of 343 families, each with a single child on the autism spectrum and at least one unaffected sibling, reveal de novo small indels and point...
Exome sequencing of 343 families, each with a single child on the autism spectrum and at least one unaffected sibling, reveal de novo small indels and point substitutions, which come mostly from the paternal line in an age-dependent manner. We do not see significantly greater numbers of de novo missense mutations in affected versus unaffected children, but gene-disrupting mutations (nonsense, splice site, and frame shifts) are twice as frequent, 59 to 28. Based on this differential and the number of recurrent and total targets of gene disruption found in our and similar studies, we estimate between 350 and 400 autism susceptibility genes. Many of the disrupted genes in these studies are associated with theĀ fragile X protein, FMRP, reinforcing links between autism and synaptic plasticity. We find FMRP-associated genes are under greater purifying selection than the remainder of genes and suggest they are especially dosage-sensitive targets of cognitive disorders.
Topics: Child; Child Development Disorders, Pervasive; Child, Preschool; Family Health; Female; Fragile X Mental Retardation Protein; Gene Dosage; Genetic Association Studies; Genetic Predisposition to Disease; Humans; Male; Models, Molecular; Mutation; Parents; Phenotype
PubMed: 22542183
DOI: 10.1016/j.neuron.2012.04.009 -
Current Osteoporosis Reports Jun 2022Review recent literature investigating the relationship between bone health and sleep/circadian disruptions (e.g., abnormal sleep duration, night shift work). (Review)
Review
PURPOSE OF REVIEW
Review recent literature investigating the relationship between bone health and sleep/circadian disruptions (e.g., abnormal sleep duration, night shift work).
RECENT FINDINGS
Short and long sleep are associated with low bone mineral density (BMD). Recent data from observational studies identified an increased risk of fracture in women with short sleep. Studies suggest that age, sex, weight change, and concurrent circadian misalignment may modify the effects of sleep restriction on bone metabolism. Interventional studies demonstrate alterations in bone metabolism and structure in response to circadian disruption that could underlie the increased fracture risk seen with night shift work. The effects of sleep and circadian disruption during adolescence may have lifelong skeletal consequences if they adversely impact bone modeling. Data suggest that short sleep and night shift work negatively impact bone metabolism and health. Rigorous studies of prevalent sleep and circadian disruptions are needed to determine mechanisms and develop prevention strategies to optimize lifelong skeletal health.
Topics: Bone Density; Bone and Bones; Female; Humans; Sleep
PubMed: 35488985
DOI: 10.1007/s11914-022-00733-y -
Clinics in Sports Medicine Jan 2021After a concussion, a series of complex, overlapping, and disruptive events occur within the brain, leading to symptoms and behavioral dysfunction. These events include... (Review)
Review
After a concussion, a series of complex, overlapping, and disruptive events occur within the brain, leading to symptoms and behavioral dysfunction. These events include ionic shifts, damaged neuronal architecture, higher concentrations of inflammatory chemicals, increased excitatory neurotransmitter release, and cerebral blood flow disruptions, leading to a neuronal crisis. This review summarizes the translational aspects of the pathophysiologic cascade of postconcussion events, focusing on the role of excitatory neurotransmitters and ionic fluxes, and their role in neuronal disruption. We review the relationship between physiologic disruption and behavioral alterations, and proposed treatments aimed to restore the balance of disrupted processes.
Topics: Athletic Injuries; Brain Concussion; Humans; Neuroimaging
PubMed: 33187612
DOI: 10.1016/j.csm.2020.08.001 -
Science Advances Aug 2015Eukaryotic replication disrupts each nucleosome as the fork passes, followed by re-assembly of disrupted nucleosomes and incorporation of newly synthesized histones into...
Eukaryotic replication disrupts each nucleosome as the fork passes, followed by re-assembly of disrupted nucleosomes and incorporation of newly synthesized histones into nucleosomes in the daughter genomes. In this review, we examine this process of replication-coupled nucleosome assembly to understand how characteristic steady state nucleosome landscapes are attained. Recent studies have begun to elucidate mechanisms involved in histone transfer during replication and maturation of the nucleosome landscape after disruption by replication. A fuller understanding of replication-coupled nucleosome assembly will be needed to explain how epigenetic information is replicated at every cell division.
PubMed: 26269799
DOI: 10.1126/sciadv.1500587 -
Annals of Operations Research Nov 2022In this study, we develop a reliable formulation based on a container network flow problem, along with the full implementation of an empty container management strategy...
In this study, we develop a reliable formulation based on a container network flow problem, along with the full implementation of an empty container management strategy in the context of an integer linear programming model. The proposed approach can play a key role in coping with disruption in the network and can offer a proactive measure for effective disruption management to maintain a stable level of reliability in supply capability. To formulate a reliable container network problem, we design the pattern of disruption, a rare and irregular uncertainty, based on binomial coefficients in the objective function. In this way, flow interruption due to disruption can be expressed in node- and arc-failures and can be properly managed. Furthermore, we provide a non-disruptive model based on a deterministic formulation derived from a bast-case scenario. Through numerical illustrations and sensitivity analyses, we conduct in-depth analyses on the impact of disruption in the container supply chain, and a benchmark model based on a bast-case scenario is used to determine disruption costs, for comparative study. In particular, the numerical experiments show that if both maritime and hinterland disruptions are not managed in advance, disruption costs derived from a benchmark model result in a significant surge according to increasing potential disruption risk. Throughout computational experiments, we also found that maritime disruption is more destructive to container supply capability than hinterland disruption is. In particular, critical findings show that when a certain level of threshold is violated, the proposed strategies are completely interrupted in a container supply chain. Therefore, proactive measures to keep up a reliability of container supply in a high-risk region are highly recommended for management side.
PubMed: 36467005
DOI: 10.1007/s10479-022-05068-6 -
Frontiers in Neuroscience 2015Perinatal exposure to endocrine disrupting chemicals (EDCs) can induce promiscuous neurobehavioral disturbances. Bisphenol A and phthalates are two widely prevalent and... (Review)
Review
Perinatal exposure to endocrine disrupting chemicals (EDCs) can induce promiscuous neurobehavioral disturbances. Bisphenol A and phthalates are two widely prevalent and persistent EDCs reported to lead to such effects. Parental and social behaviors are especially vulnerable to endocrine disruption, as these traits are programmed by the organizational-activational effects of testosterone and estrogen. Exposure to BPA and other EDCs disrupts normal maternal care provided by rodents and non-human primates, such as nursing, time she spends hunched over and in the nest, and grooming her pups. Paternal care may also be affected by BPA. No long-term study has linked perinatal exposure to BPA or other EDC and later parental behavioral deficits in humans. The fact that the same brain regions and neural hormone substrates govern parental behaviors in animal models and humans suggests that this suite of behaviors may also be vulnerable in the latter. Social behaviors, such as communication, mate choice, pair bonding, social inquisitiveness and recognition, play behavior, social grooming, copulation, and aggression, are compromised in animal models exposed to BPA, phthalates, and other EDCs. Early contact to these chemicals is also correlated with maladaptive social behaviors in children. These behavioral disturbances may originate by altering the fetal or adult gonadal production of testosterone or estrogen, expression of ESR1, ESR2, and AR in the brain regions governing these behaviors, neuropeptide/protein hormone (oxytocin, vasopressin, and prolactin) and their cognate neural receptors, and/or through epimutations. Robust evidence exists for all of these EDC-induced changes. Concern also exists for transgenerational persistence of such neurobehavioral disruptions. In sum, evidence for social and parental deficits induced by BPA, phthalates, and related chemicals is strongly mounting, and such effects may ultimately compromise the overall social fitness of populations to come.
PubMed: 25784850
DOI: 10.3389/fnins.2015.00057 -
Experientia Supplementum (2012) 2012Mammalian reproductive tract development is a tightly regulated process that can be disrupted following exposure to drugs, toxicants, endocrine-disrupting chemicals... (Review)
Review
Mammalian reproductive tract development is a tightly regulated process that can be disrupted following exposure to drugs, toxicants, endocrine-disrupting chemicals (EDCs), or other compounds via alterations to gene and protein expression or epigenetic regulation. Indeed, the impacts of developmental exposure to certain toxicants may not be fully realized until puberty or adulthood when the reproductive tract becomes sexually mature and altered functionality is manifested. Exposures that occur later in life, once development is complete, can also disrupt the intricate hormonal and paracrine interactions responsible for adult functions, such as spermatogenesis. In this chapter, the biology and toxicology of the male reproductive tract is explored, proceeding through the various life stages including in utero development, puberty, adulthood, and senescence. Special attention is given to the discussion of EDCs, chemical mixtures, low-dose effects, transgenerational effects, and potential exposure-related causes of male reproductive tract cancers.
Topics: Aging; Animals; Endocrine Disruptors; Environmental Exposure; Environmental Pollutants; Genitalia, Male; Humans; Male; Neoplasms, Germ Cell and Embryonal; Prostatic Diseases; Puberty; Reproduction; Testicular Neoplasms
PubMed: 22945574
DOI: 10.1007/978-3-7643-8340-4_11