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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 -
Advances in Nutrition (Bethesda, Md.) Jan 2020The intestinal tract is the largest barrier between a person and the environment. In this role, the intestinal tract is responsible not only for absorbing essential... (Review)
Review
The intestinal tract is the largest barrier between a person and the environment. In this role, the intestinal tract is responsible not only for absorbing essential dietary nutrients, but also for protecting the host from a variety of ingested toxins and microbes. The intestinal barrier system is composed of a mucus layer, intestinal epithelial cells (IECs), tight junctions (TJs), immune cells, and a gut microbiota, which are all susceptible to external factors such as dietary fats. When components of this barrier system are disrupted, intestinal permeability to luminal contents increases, which is implicated in intestinal pathologies such as inflammatory bowel disease, necrotizing enterocolitis, and celiac disease. Currently, there is mounting evidence that consumption of excess dietary fats can enhance intestinal permeability differentially. For example, dietary fat modulates the expression and distribution of TJs, stimulates a shift to barrier-disrupting hydrophobic bile acids, and even induces IEC oxidative stress and apoptosis. In addition, a high-fat diet (HFD) enhances intestinal permeability directly by stimulating proinflammatory signaling cascades and indirectly via increasing barrier-disrupting cytokines [TNFα, interleukin (IL) 1B, IL6, and interferon γ (IFNγ)] and decreasing barrier-forming cytokines (IL10, IL17, and IL22). Finally, an HFD negatively modulates the intestinal mucus composition and enriches the gut microflora with barrier-disrupting species. Although further research is necessary to understand the precise role HFDs play in intestinal permeability, current data suggest a stronger link between diet and intestinal disease than was first thought to exist. Therefore, this review seeks to highlight the various ways an HFD disrupts the gut barrier system and its many implications in human health.
Topics: Animals; Bile Acids and Salts; Cytokines; Diet, High-Fat; Dietary Fats; Gastrointestinal Microbiome; Gastrointestinal Tract; Humans; Inflammation; Intestinal Mucosa; Mucus; Permeability; Tight Junctions
PubMed: 31268137
DOI: 10.1093/advances/nmz061 -
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 -
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 -
International Journal of Molecular... Feb 2023Availability of artificial light and light-emitting devices have altered human temporal life, allowing 24-hour healthcare, commerce and production, and expanding social... (Review)
Review
Availability of artificial light and light-emitting devices have altered human temporal life, allowing 24-hour healthcare, commerce and production, and expanding social life around the clock. However, physiology and behavior that evolved in the context of 24 h solar days are frequently perturbed by exposure to artificial light at night. This is particularly salient in the context of circadian rhythms, the result of endogenous biological clocks with a rhythm of ~24 h. Circadian rhythms govern the temporal features of physiology and behavior, and are set to precisely 24 h primarily by exposure to light during the solar day, though other factors, such as the timing of meals, can also affect circadian rhythms. Circadian rhythms are significantly affected by night shift work because of exposure to nocturnal light, electronic devices, and shifts in the timing of meals. Night shift workers are at increased risk for metabolic disorder, as well as several types of cancer. Others who are exposed to artificial light at night or late mealtimes also show disrupted circadian rhythms and increased metabolic and cardiac disorders. It is imperative to understand how disrupted circadian rhythms alter metabolic function to develop strategies to mitigate their negative effects. In this review, we provide an introduction to circadian rhythms, physiological regulation of homeostasis by the suprachiasmatic nucleus (SCN), and SCN-mediated hormones that display circadian rhythms, including melatonin and glucocorticoids. Next, we discuss circadian-gated physiological processes including sleep and food intake, followed by types of disrupted circadian rhythms and how modern lighting disrupts molecular clock rhythms. Lastly, we identify how disruptions to hormones and metabolism can increase susceptibility to metabolic syndrome and risk for cardiovascular diseases, and discuss various strategies to mitigate the harmful consequences associated with disrupted circadian rhythms on human health.
Topics: Humans; Circadian Rhythm; Suprachiasmatic Nucleus; Sleep; Melatonin; Eating; Circadian Clocks; Light
PubMed: 36834801
DOI: 10.3390/ijms24043392 -
Trends in Neurosciences Oct 2023Postmitotic neurons require persistently active controls to maintain terminal differentiation. Unlike dividing cells, aberrant cell cycle activation in mature neurons... (Review)
Review
Postmitotic neurons require persistently active controls to maintain terminal differentiation. Unlike dividing cells, aberrant cell cycle activation in mature neurons causes apoptosis rather than transformation. In Alzheimer's disease (AD) and related tauopathies, evidence suggests that pathogenic forms of tau drive neurodegeneration via neuronal cell cycle re-entry. Multiple interconnected mechanisms linking tau to cell cycle activation have been identified, including, but not limited to, tau-induced overstabilization of the actin cytoskeleton, consequent changes to nuclear architecture, and disruption of heterochromatin-mediated gene silencing. Cancer- and development-associated pathways are upregulated in human and cellular models of tauopathy, and many tau-induced cellular phenotypes are also present in various cancers and progenitor/stem cells. In this review, I delve into mechanistic parallels between tauopathies, cancer, and development, and highlight the role of tau in cancer and in the developing brain. Based on these studies, I put forth a model by which pathogenic forms of tau disrupt the program that maintains terminal neuronal differentiation, driving cell cycle re-entry and consequent neuronal death. This framework presents tauopathies as conditions involving the profound toxic disruption of neuronal identity.
Topics: Humans; Alzheimer Disease; Tauopathies; Neurons; Brain; Stem Cells
PubMed: 37591720
DOI: 10.1016/j.tins.2023.07.006