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1.
Int J Geriatr Psychiatry ; 38(10): e6010, 2023 10.
Article in English | MEDLINE | ID: mdl-37794769

ABSTRACT

OBJECTIVES: The proportion of older people with dementia in China is gradually increasing with the increase in the aging population over recent years. Hypertension and diabetes are common non-communicable diseases among rural populations in China. However, it remains unclear whether these conditions affect the occurrence and development of cognitive impairment as there is limited research on cognitive status and its risk factors among residents of rural areas. METHODS: A multi-stage stratified cluster random sampling method was used to select 5400 participants from rural permanent residents. A self-designed structured questionnaire was used to investigate demographic data of the participants. Cognitive function was assessed using the Montreal Cognitive Function Assessment Scale (MoCA). The results were analyzed using chi-square test, ANOVA and multiple linear regression analysis. RESULTS: A total of 5028 participants returned the survey, giving a response rate of 93.1%. Higher education (odds ratio (OR) = 3.2, 95% confidence interval (CI) 2.87-3.54, p < 0.001), higher income (OR = 1.61, 95% CI 1.16-2.07, p < 0.001), and dietary control (OR = 0.66, 95%CI 0.34-0.98, p < 0.001) were protective factors. A visual representation of the relationship between annual income and MoCA score showed an inverted U-curve, the group with an annual income of 6000-7999 RMB had a maximum OR of 1.93 (95%CI 0.12-2.74, p < 0.001). While difficulty in maintaining sleep were risk factors for cognitive impairment (OR = -2.28, 95% CI-4.18-0.39, p = 0.018). CONCLUSIONS: Participants with middle incomes had better cognitive status than those with the highest incomes. Higher education, proper diet control and good sleep are beneficial to the cognitive status of residents in rural areas.


Subject(s)
Diabetes Mellitus , Hypertension , Humans , Aged , Cross-Sectional Studies , Rural Population , Risk Factors , Hypertension/epidemiology , Cognition , China/epidemiology
2.
Toxicol Ind Health ; 39(2): 104-114, 2023 Feb.
Article in English | MEDLINE | ID: mdl-36617730

ABSTRACT

Aluminum (Al) is a common neurotoxic element that can exacerbate intracellular ß-amyloid (Aß) deposition. Reelin is a highly conserved extracellular glycoprotein that is involved in intracellular Aß deposition. However, the action of Reelin on aluminum-induced Aß deposition is not fully understood. Here, we investigated the effects of the Reelin-Dab1 signaling pathway on Aß deposition in aluminum maltol (Al(mal)3) exposure in rat pheochromocytoma-derived cells (PC12). Our results showed that Al(mal)3 exposure decreased activity of PC12, increased expression of Aß42, and decreased expression of Aß40. Moreover, Al(mal)3 exposure in PC12 induced Reelin-Dab1 signaling pathway-associated proteins changed, decreased expression of Reelin and Dab1, and increased expression of pdab1. Moreover, the expression of Reelin, Dab1, and Aß40 was found to be elevated in PC12 exposed to Al(mal)3 and corticosterone compared to those exposed to Al(mal)3. Also, the expression of Reelin, Dab1, and Aß40 was found to be depressed in PC12 exposed to Al(mal)3 and streptozotocin compared with cells exposed to Al(mal)3 alone. These results suggested that Al(mal)3 inhibits the expression of the Reelin-Dab1 signaling pathway, promoting Aß deposition. Thus, our findings provided important evidence to better understand how the Reelin-Dab1 signaling pathway may be a potential mechanism of Aß deposition induced by aluminum.


Subject(s)
Aluminum , Extracellular Matrix Proteins , Animals , Rats , Aluminum/toxicity , Cell Adhesion Molecules, Neuronal/genetics , Cell Adhesion Molecules, Neuronal/metabolism , Extracellular Matrix Proteins/metabolism , Serine Endopeptidases/genetics , Serine Endopeptidases/metabolism , Signal Transduction , Amyloid beta-Peptides/metabolism
3.
Toxicol Mech Methods ; 32(7): 530-541, 2022 Sep.
Article in English | MEDLINE | ID: mdl-35313783

ABSTRACT

Aluminum (Al), a neurotoxic element, can induce Alzheimer's disease-like (AD-like) changes by triggering neuronal death. Iron homeostasis disturbance has also been implicated in Alzheimer's disease (AD), and excess iron exacerbates oxidative damage and cognitive defects. Ferroptosis is a nonapoptotic form of cell death dependent upon intracellular iron. However, the involvement of neuronal death induced by aluminum maltolate (Al(mal)3) in the pathogenesis of AD remains elusive. In this study, the results of three different behavioral experiments suggested that the learning and memory ability deteriorated and autonomous activity declined of these rats that exposed Al(mal)3 were alleviated by deferoxamine (DFO). Transmission electron microscope observations showed that the membrane was ruptured, and the membrane density increased and ridge disappearance (the most prominent characteristic of ferroptosis) in the perinuclear and cytoplasmic compartments of the hippocampal neurons were perceived in the exposure group, while the DFO group and 18 µM/kg Al(mal)3+DFO group were alleviated compared with 18 µM/kg Al(mal)3. In addition, DFO prevented oxidative stress, such as increased glutathione (GSH) and decreased malondialdehyde (MDA) and reactive oxygen species (ROS), while the latter two indexes had the same changing tendency as the total iron of brain tissue. These data indicated that Al(mal)3 could cause ferroptosis in Sprague-Dawley (SD) rat neurons, which was inhibited by DFO via reducing the content of iron and increasing the ability of cells to resist oxidative damage.


Subject(s)
Alzheimer Disease , Ferroptosis , Aluminum/toxicity , Animals , Brain/metabolism , Deferoxamine/metabolism , Deferoxamine/pharmacology , Iron/metabolism , Iron/toxicity , Iron Chelating Agents/metabolism , Iron Chelating Agents/pharmacology , Neurons/metabolism , Oxidative Stress , Rats , Rats, Sprague-Dawley
4.
Toxicol Mech Methods ; 31(1): 33-42, 2021 Jan.
Article in English | MEDLINE | ID: mdl-32900247

ABSTRACT

Aluminum (Al), a neurotoxic element, can induce Alzheimer's disease (AD) via triggering neuronal death. Ferroptosis is a new type of programmed cell death related to neurological diseases. Unfortunately, its role in aluminum-induced neuronal death remains completely unclear. This study aimed to investigate whether ferroptosis is involved in neuronal death in response to aluminum exposure as well as its underlying mechanism. In this study, rat adrenal pheochromocytoma (PC12) cells were treated with 200 µM aluminum maltolate (Al(mal)3) for 24 h, and related biochemical indicators were assessed to determine whether ferroptosis was induced by aluminum in neurons. Then, the potential mechanism was explored by detecting of these genes and proteins associated with ferroptosis after adding ferroptosis-specific agonist Erastin (5 µM) and antagonist Ferrostatin-1 (Fer-1) (5 µM). The experimental results demonstrated that aluminum exposure significantly increased the death of PC12 cells and caused specific mitochondrial pathological changes of ferroptosis in PC12 cells. Further research confirmed that ferroptosis was triggered by aluminum in PC12 cells by means of activating the oxidative damage signaling pathway, which was displayed as inhibition of the cysteine/glutamate antiporter system (system Xc-), causing the depletion of cellular glutathione (GSH) and inactivation of glutathione peroxidase (GSH-PX) eventually lead to accumulation of reactive oxygen species (ROS). Taken together, ferroptosis was a means of neuronal death induced by aluminum and oxidative damage may be its underlying mechanism, which also provided some new clues to potential target for the intervention and therapy of AD.


Subject(s)
Ferroptosis/drug effects , Mitochondria/drug effects , Neurons/drug effects , Organometallic Compounds/toxicity , Oxidative Stress/drug effects , Pyrones/toxicity , Animals , Mitochondria/metabolism , Mitochondria/ultrastructure , Neurons/metabolism , Neurons/ultrastructure , PC12 Cells , Rats , Reactive Oxygen Species/metabolism , Signal Transduction
5.
Nurs Health Sci ; 18(2): 223-9, 2016 Jun.
Article in English | MEDLINE | ID: mdl-26755351

ABSTRACT

This cross-sectional comparative study investigated the levels of insomnia, anxiety, and heart rate variability of nurses members working different shift systems. One hundred and twenty-four participants were recruited from members of the nurses of two Taiwanese hospitals. Data were collected using the Chinese versions of the Athens Insomnia Scale and Beck Anxiety Scale questionnaires and electrocardiograms recorded immediately upon completion of each participant's work shift. A binary logistic regression model was used for analysis. Insomnia, anxiety, and abnormal parasympathetic activity were more acute in nurses who worked a rotating shift than in those performing day or night shift work. Logistic regression analysis showed that age significantly increased the incidence and level of insomnia. Age, years of service, and nurses' status as a parent significantly intensified incidences of anxiety and abnormal parasympathetic activity. Rotating shift work is one of the main factors causing adverse effects on the physical and psychological health of nurses; therefore, when a shift work system cannot be avoided, a practice of day and night shifts for nurses is preferable to rotating shifts.


Subject(s)
Anxiety/psychology , Heart Rate , Nurses/psychology , Sleep Initiation and Maintenance Disorders/psychology , Work Schedule Tolerance/psychology , Adult , Anxiety/etiology , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Nurses/statistics & numerical data , Sleep Disorders, Circadian Rhythm/complications , Sleep Disorders, Circadian Rhythm/psychology , Sleep Initiation and Maintenance Disorders/etiology , Taiwan
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