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Background: The population aged 80 or over has increased, which may predispose people to dementia. Validated scales are used to diagnose them. The study aimed to compare cognitive evolution and associated factors in individuals aged 80 or over. Method: The Research Ethics Committee from the University of Southern Santa Catarina (UNESC) authorized the study under 3,214,698. It was an observational, quantitative study with a cohort design. Individuals aged 80 or over were recruited for this study. One hundred twenty‐four participants were evaluated in 2016. After six years, they were reevaluated, with 102 participants lost to follow‐up, resulting in 22 participants for reapplication. In addition, 78 new participants entered the study, totaling 100 participants in 2022. Cognitive tests such as the Mini‐Mental State Examination (MMSE), Clock Test, Verbal Fluency, and Montreal Cognitive Assessment (MOCA) were applied. Result: When comparing the two times, there was a significant difference in the percentage of retirement and participation in some activities in the community. Compared to cognitive tests, a decrease in cognitive decline and verbal fluency was observed in 2022, assessed by the MMSE. When the 22 individuals were evaluated over six years, there was a significant change in participation in community activities. When asked about difficulty remembering things, people, or situations, there was a reduction in 2022. Unlike the MMSE and the verbal fluency test, the MOCA showed cognitive impairment in most individuals in 2022. Conclusion: It is concluded that the population of 2016 and 2022 showed some differences related to cognition, but this difference was not observed in the 22 individuals. These results indicate a divergence between the tests. Considering the many differences in the Brazilian population, it is necessary to standardize a cognitive test suitable for screening cognitive decline. [ABSTRACT FROM AUTHOR]

Background: Aging is a natural, irreversible process that can be successful or pathological, resulting in chronic degenerative diseases such as Alzheimer's disease. Low levels of estrogen characterize menopause. Research reveals that the lack of these hormones may be related to dementia and that vitamin D (vit D), when supplemented, has a neuroprotective and neuromodulator effect. Method: 60‐ or 120‐day‐old Wistar rats were subjected to ovariectomy (OVX) for either 1 or 8 months, treatment with oral administration of Vit D (42 or 420 IU/kg) and/or DONE (1 mg/kg) spanned 21 days. On the 22nd day of the protocol, 24 hours post the final administration, the prefrontal cortex and hippocampus were dissected for cytokine analysis, including interleukin 10 (IL‐10), IL‐1 β, and tumor necrosis factor α (TNF‐ α), conducted through enzyme immunoassay. Result: In 60‐day‐old rats undergoing one month of ovariectomy (OVX), elevated IL‐1β and TNF‐α levels were observed in the brain. The optimal dose for mitigating these effects was found to be vitamin D (Vit D) at 420 IU/kg, either alone or in combination with DONE. This dosage successfully reversed the increased IL‐1β levels in the frontal cortex and normalized the elevated TNF‐α levels in the hippocampus. Similarly, in rats subjected to OVX for eight months, the most effective dose for reversing increased IL‐1β levels in the frontal cortex and hippocampus was Vit D at 420 IU/kg. However, in this protocol, TNF‐α levels remained unchanged, emphasizing the selective impact of this particular dosage. Additionally, the optimal dose for modulating IL‐10 levels in the frontal cortex, particularly in the context of increased IL‐10 following OVX, was Vit D at 420 IU/kg. Conclusion: The administration of vitamin D either alone or in combination with DONE (a specific treatment) demonstrated favorable outcomes in the rats, effectively mitigating the inflammatory response. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease. The animal model of AD‐like dementia induced by the peptide β‐amyloid 1‐42 (Aβ1‐42) is widely used. However, the animals have to be anesthetized and no studies are evaluating which anesthetic causes less interference in this model. This study aimed to evaluate the interference of different anesthetics on behavioral and oxidative stress in a mice model of Aβ1‐42‐induced dementia. Method: Male and female BALB/c mice at 3‐ month‐old were used under three different protocols. Protocol 1 (inhalation): (1) 100% oxygen (isoflurane control); (2) artificial cerebrospinal fluid (ACSF) + isoflurane; (3) Aβ1‐42 + isoflurane. Protocol 2 (intraperitoneal): (1) saline; (2) ACSF + ketamine + xylazine; (3) ACSF + ketamine + dexmedetomidine; (4) Aβ1‐42 + ketamine + xylazine; (5) Aβ1‐42 + ketamine + dexmedetomidine. Protocol 3 (intraperitoneal): (1) saline; (2) ACSF + propofol; (3) Aβ1‐42 + propofol. After the anesthesia, mice were injected with Aβ1‐42 (400 pmol) free‐hand intracerebroventricular, then after 13 days, mice were submitted to the Y‐maze test (spatial memory), plus‐maze (anxiety), and open‐field (habituation memory); then, hippocampus were dissected to analysis. Result: Isoflurane per se (protocol 1) caused no memory impairment, but caused an anxiolytic effect in males, in addition, to increased sulfhydryl content in males. In protocol 2, ACSF + ketamine + xylazine induced spatial memory impairment in males and habituation memory impairment in females; the anesthetics of protocol 2 increased 2',7' dichlorodihydrofluorescein (DCF) levels in females, and ACSF + ket + dex reduced levels of glutathione (GSH) in males. In protocol 3, propofol per se caused an anxiolytic effect in males and increased DCF levels in males and females, increased superoxide dismutase activity in males, and reduction in females, in addition, increased sulfhydryl content in males. Conclusion: All anesthetic protocols evaluated caused alterations in the behavior and/or oxidative stress parameters; however, isoflurane seems to cause less interference in the animal model, followed by propofol. Protocol 3 seems to cause more interference, including in the Y‐maze (spatial memory), which is one of the main behavior tests to evaluate the mice model of Aβ1‐42‐induced dementia. [ABSTRACT FROM AUTHOR]