Association of nighttime light and cognitive function among middle-aged and older Chinese adults：A 9-Year Longitudinal Study DOI Creative Commons
Ting Tang, Meijin Zhang, Xiaodong Pan

и другие.

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Окт. 18, 2024

Abstract Background Nighttime Lights (NTLs) data represent records of artificial light emissions from human activities, used to analyze socioeconomic development. However, studies have found that long-term exposure nighttime pollution may significantly impact cognitive function. Thus, we extensively reviewed published time-series NTLs datasets investigate the risk dysfunction in populations. Methods The study utilized China Health and Retirement Longitudinal Study (CHARLS) NPP/VIIRS (NTL) data. We employed latent class trajectory modeling identify 9-year trajectories NTL assessed participants' function initially 2020. Logistic regression models were assess associated with different trajectories. potential mediating effect sleep duration on relationship between was also explored. Results A dose–response observed baseline lights impairment. Restricted cubic spline demonstrated a non-linear (U-shaped) impairment (p for non-linearity < 0.001). Sleep mediated this accounted 2.1% total variance. Two identified. Multiple logistic analysis indicated reduced low-intensity lighting group (OR: 0.73, p Conclusions impaired cognition varied across trajectories, overall by duration. These findings potentially establish connection environmental indicators

Язык: Английский

The glymphatic system and Amyotrophic lateral sclerosis DOI
Andrew Eisen, Maiken Nedergaard,

E. G. Gray

и другие.

Progress in Neurobiology, Год журнала: 2024, Номер 234, С. 102571 - 102571

Опубликована: Янв. 22, 2024

Язык: Английский

Процитировано

8
Proteostasis disruption and senescence in Alzheimer’s disease pathways to neurodegeneration DOI
Riya Thapa, Asif Ahmad Bhat, Moyad Shahwan

и другие.

Brain Research, Год журнала: 2024, Номер 1845, С. 149202 - 149202

Опубликована: Авг. 30, 2024

Язык: Английский

Процитировано

8
TDP-43 as a potential retinal biomarker for neurodegenerative diseases DOI Creative Commons
Margit Glashutter, Printha Wijesinghe, Joanne A. Matsubara

и другие.

Frontiers in Neuroscience, Год журнала: 2025, Номер 19

Опубликована: Фев. 12, 2025

TDP-43 proteinopathies are a spectrum of neurodegenerative diseases (NDDs) characterized by the pathological cytoplasmic aggregation protein. These include amyotrophic lateral sclerosis (ALS), frontotemporal lobar degeneration (FTLD), Alzheimer’s disease (AD), chronic traumatic encephalopathy (CTE), and others. in eye shows promise as biomarker for these NDDs. Several studies have identified inclusions retinal layers donors with ALS, FTLD, AD, CTE, other conditions using immunohistochemistry. Our findings suggest that aggregates human retina most prevalent FTLD-TDP, suggesting may provide reliable context studying potential biomarker. Animal model been pivotal exploring TDP-43’s roles retina, including its nuclear localization, RNA binding properties, interactions proteins. Despite advances, more research is needed to develop therapeutic strategies. A major limitation autopsy lack corresponding brain pathology assessments confirm proteinopathy diagnosis staging. Other limitations small sample sizes, antemortem clinical histories, limited comparisons across multiple Future directions NDDs tracers, hyperspectral imaging, oculomics, machine learning development.

Язык: Английский

Процитировано

1
Sleep and Oxidative Stress: Current Perspectives on the Role of NRF2 DOI Creative Commons
Sergio Davinelli, Alessandro Medoro, Rosa Savino

и другие.

Cellular and Molecular Neurobiology, Год журнала: 2024, Номер 44(1)

Опубликована: Июнь 25, 2024

Abstract Sleep is a fundamental conserved physiological state across evolution, suggesting vital biological functions that are yet to be fully clarified. However, our understanding of the neural and molecular basis sleep regulation has increased rapidly in recent years. Among various processes implicated controlling homeostasis, bidirectional relationship between oxidative stress recently emerged. One proposed function may mitigation both brain peripheral tissues, contributing clearance reactive species accumulate during wakefulness. Conversely, species, such as oxygen (ROS) nitrogen (RNS), at levels, act signaling agents regulate redox-sensitive transcriptional factors, enzymes, other effectors involved sleep. As primary sensor intracellular oxidation, transcription factor NRF2 emerging an indispensable component maintain cellular redox homeostasis Indeed, number studies have revealed association dysfunction most common conditions, including loss, obstructive apnea, circadian disturbances. This review examines evidence intricate link context sleep, highlights potential modulators alleviate Graphical A been shown, indicating play protective role against accumulation wakefulness deprivation. might also serve molecules influence mechanisms. Notably, changes, key regulator homeostasis.

Язык: Английский

Процитировано

6
Serotonergic dysfunction may mediate the relationship between alcohol consumption and Alzheimer’s disease DOI Creative Commons
Samantha Pierson, Louis J. Kolling, Thomas D. James

и другие.

Pharmacological Research, Год журнала: 2024, Номер 203, С. 107171 - 107171

Опубликована: Апрель 9, 2024

The impact of Alzheimer's disease (AD) and its related dementias is rapidly expanding, mitigation remains an urgent social technical challenge. To date there are no effective treatments or interventions for AD, but recent studies suggest that alcohol consumption correlated with the risk developing dementia. In this review, we synthesize data from preclinical, clinical, epidemiological models to evaluate combined role serotonergic dysfunction in underscoring need further research on topic. We first discuss limitations inherent current data-collection methods, how neuropsychiatric symptoms common among use disorder, may mask their co-occurrence. additionally describe excess accelerate development AD via direct effects function, explore roles neuroinflammation proteostasis mediating relationship between serotonin, consumption, AD. Lastly, argue a shift disentangle pathogenic early-affected brainstem structures

Язык: Английский

Процитировано

4
SLEEP DISORDERS AND RISK OF ALZHEIMER'S DISEASE: A TWO-WAY ROAD DOI

Rafael Antônio Vicente Lacerda,

Janaína Aparecida Favero Desio, Camila Marciele Kammers

и другие.

Ageing Research Reviews, Год журнала: 2024, Номер unknown, С. 102514 - 102514

Опубликована: Сен. 1, 2024

Язык: Английский

Процитировано

4
Cellular and humoral mechanisms of immunosenescence DOI Creative Commons
I. V. Nesterova, С. В. Ковалева, Г. А. Чудилова

и другие.

Cytokines and inflammation, Год журнала: 2025, Номер unknown

Опубликована: Янв. 23, 2025

Despite the success achieved in increasing average life expectancy, problems of improving quality elderly and old people, prevention therapy age-associated diseases geriatric syndromes are still relevant. The immune system plays a key role aging process, functioning which undergoes wide range changes, collectively called "immunosenescence". Aging cells is associated with shortening telomeric regions chromosomes, loss protein homeostasis (proteostasis), mitochondrial dysfunction, DNA damage, oxidative stress. Senescent marked by resistance to apoptosis, cell cycle arrest abnormal production proinflammatory cytokines, leading development chronic low-grade inflammation. In this case, effector mechanisms response depleted, accompanied low ability adequately respond an antigenic stimulus. Thymus atrophy, depletion bone marrow niches, myeloid bias hematopoiesis change ratio lymphocyte subsets occur. addition, functions neutrophilic granulocytes impaired, but nature their during immunosenescence has not been sufficiently studied, so additional studies needed establish granulocyte dysfunctions immunosenescence.

Язык: Английский

Процитировано

0
Melatonin regulation of phase separation in Neuro-PASC: out-maneuvering Janus-faced amyloids DOI Creative Commons
Doris Loh, Russel J. Reıter

Exploration of neuroscience, Год журнала: 2025, Номер 4

Опубликована: Март 24, 2025

The SAR-CoV-2 virus has evolved to co-exist with human hosts, albeit at a substantial energetic cost resulting in post-infection neurological manifestations [Neuro-post-acute sequelae of SARS-CoV-2 infection (PASC)] that significantly impact public health and economic productivity on global scale. One the main molecular mechanisms responsible for development Neuro-PASC, individuals all ages, is formation inadequate proteolysis/clearance phase-separated amyloid crystalline aggregates—a hallmark feature aging-related neurodegenerative disorders. Amyloidogenesis during viral persistence natural, inevitable, protective defense response exacerbated by SARS-CoV-2. Acting as chemical catalyst, accelerates hydrophobic collapse heterogeneous nucleation amorphous amyloids into stable β-sheet aggregates. clearance aggregates most effective slow wave sleep, when high levels adenosine triphosphate (ATP)—a biphasic modulator biomolecular condensates—and melatonin are available solubilize removal. dysregulation mitochondrial dynamics SARS-CoV-2, particular fusion fission homeostasis, impairs proper distinct subpopulations can remedy challenges created diversion substrates away from oxidative phosphorylation towards glycolysis support replication maintenance. subsequent reduction ATP inhibition synthesis sleep results incomplete brain aggregates, leading commonly associated age-related Exogenous not only prevents dysfunction but also elevates production, effectively augmenting solubilizing effect moiety ensure timely, optimal disaggregation pathogenic prevention attenuation Neuro-PASC.

Язык: Английский

Процитировано

0
Exploring the nexus: Sleep disorders, circadian dysregulation, and Alzheimer’s disease DOI
Pratima Khandayataray, Meesala Krishna Murthy

Neuroscience, Год журнала: 2025, Номер unknown

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0
Tauopathy after long‐term cervical lymphadenectomy DOI Creative Commons
Chenrui Wu, Jiangyuan Yuan, Yu Tian

и другие.

Alzheimer s & Dementia, Год журнала: 2025, Номер 21(4)

Опубликована: Апрель 1, 2025

Abstract INTRODUCTION This study examined the effects of long‐term cervical lymphadenectomy (cLE) on cognitive and Alzheimer's disease (AD)–like tauopathy changes. METHODS Male C57BL/6 mice were used to assess cLE impacts sleep, brain pathways, pathologies. RNA sequencing proteomics analyzed gene/protein changes, with results verified by western blotting immunofluorescence. RESULTS CLE led sleep psychiatric disorders, linked mitogen‐activated protein kinase/extracellular signal‐regulated kinase (ERK) pathway activation. Activation ERK may interfere autophagy is associated phosphorylated tau accumulation. Peripheral blood analysis shows decreased waste in peripheral post‐cLE, implicating impaired lymphatic drainage build‐up. DISCUSSION These findings suggest a potential connection between AD‐like tauopathy, potentially influencing surgical decisions. Highlights Cervical cornerstone head neck cancers, affecting millions people each year. We provide first evidence mildly functioning significant anxiety–depressive disorders after cLE. Long‐term not only directly impairs wastes (amyloid beta, [p‐tau]) drainage, but also activates Erk1/2 signaling leading attenuation autophagy. found for time that accelerated deposition p‐tau young mice. Patients clinical lymph node dissection showed reduced consistent mouse models. suggests need further evaluation neurologic dissection, procedure affects

Язык: Английский

Процитировано

0