Aim: In this study, the protective effects of atorvastatin calcium (AC) on nerve cells and cognitive improvement and were investigated by establishing cell models and vascular dementia (VD) rat models.
Background: VD is a neurodegenerative disease characterized by cognitive deficits caused by chronic cerebral hypoperfusion. AC has been studied for its potential to cure VD but its efficacy and underlying mechanism are still unclear.
Objective: The mechanism of action of AC on cognitive deficits in the early stages of VD is unclear. Here, the 2-vessel occlusion (2-VO) model and the hypoxia/reoxygenation (H/R) cell model was established to investigate the function of AC in VD.
Methods: The spatial learning and memory abilities of rats were detected by the Morris method. The IL-6, tumour necrosis factor-α (TNF-α), malondialdehyde (MDA) and superoxide dismutase (SOD) in cell supernatant was tested by ELISA kits. After behavioural experiments, rats were anaesthetized and sacrificed, and their brains were extracted. One part was immediately fixed in 4% paraformaldehyde for H&E, Nissl, and immunohistochemical analyses, and the other was stored in liquid nitrogen. All data were shown as mean ± SD. Statistical comparison between the two groups was performed by Student's t-test. A two-way ANOVA test using GraphPad Prism 7 was applied for escape latency analysis and the swimming speed test. The difference was considered statistically significant at p < 0.05.
Results: AC decreased apoptosis, increased autophagy, and alleviated oxidative stress in primary hippocampal neurons. AC regulated autophagy-related proteins by western blotting. VD mice improved cognitively in the Morris water maze. Spatial probing tests showed that VD animals administered AC had considerably longer swimming times to the platform than VD rats. H&E and Nissl staining showed that AC reduces neuronal damage in VD rats. Western blot and qRT-PCR indicated that AC in VD rats inhibited Bax and promoted LC3-II, Beclin-1, and Bcl-2 in the hippocampus region. AC also improves cognition via the AMPK/mTOR pathway.
Conclusion: This study found that AC may relieve learning and memory deficits as well as neuronal damage in VD rats by changing the expression of apoptosis/autophagy-related genes and activating the AMPK/mTOR signalling pathway in neurons.
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http://dx.doi.org/10.2174/1386207326666230606114448 | DOI Listing |
Eur J Pediatr
December 2024
Dept. of Research and Development, SeysCentra, Malden, The Netherlands.
Unlabelled: Children with Noonan syndrome-like RASopathies are at increased risk for developing feeding problems due to comorbid organic impairments at an early age, such as gastrointestinal problems or other organicity. Their feeding problems can ultimately often be classified as avoidant/restrictive food intake disorder, for which behavioral therapy is the first-choice treatment. The research question in this study is whether this treatment leads to similar results as in children without these RASopathies.
View Article and Find Full Text PDFEur J Pediatr
December 2024
Division of Child Neurology, Department of Paediatrics, Faculty of Medicine, Eskisehir Osmangazi University, Eskisehir, Turkey.
Unlabelled: Phenylalanine (PA) levels below 360 µmol/L do not require treatment; however, cognitive deficits have been observed in patients with elevated PA levels, necessitating a safe upper limit for treatment and therapeutic objectives. The main purpose of this study is to evaluate the correlation between developmental assessments (Denver Developmental Screening Test-II [DDST-II] and Ankara Developmental Screening Inventory [ADSI]) and electroencephalogram (EEG) findings with blood PA levels and genotypic data in non-phenylketonuria mild Hyperphenylalaninemia (HPA) patients, to re-evaluate their treatment status based on potential adverse outcomes. This study encompassed 40 patients aged 1-5 years diagnosed with HPA and not on treatment, identified through initial blood PA levels, and monitored for a minimum of 1 year on an unrestricted diet.
View Article and Find Full Text PDFJ Neuroeng Rehabil
December 2024
Section of Physiology, Laboratory of Neuro-Biomechanics, Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, 95123, Catania, Italy.
Background: Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder, characterized by impairments in social interaction and communication with restricted and repetitive behavior. Postural and motor disturbances occur more often in ASD, in comparison to typically developing subjects, affecting the quality of life. Linear and non-linear indexes derived from the trajectory of the center of pressure (COP) while subjects stand on force platforms are commonly used to assess postural stability.
View Article and Find Full Text PDFCereb Cortex
December 2024
Department of Neurology, Xuanwu Hospital of Capital Medical University, #45 Changchun Street, Xicheng District, Beijing 100053, China.
The asymmetric pattern of β-amyloid plaque distribution across Alzheimer's disease clinical progression stages remains unclear. In this study, 66 participants with normal cognition, 59 with subjective cognitive decline, 12 with mild cognitive impairment, and 11 with Alzheimer's disease dementia were included in the Sino Longitudinal Study on Cognitive Decline (SILCODE) cohort. A regional asymmetry index, denoting the left-right asymmetry of β-amyloid plaques, was derived for each region based on the Anatomical Automatic Labeling atlas.
View Article and Find Full Text PDFJ Child Psychol Psychiatry
December 2024
School of Academic Psychiatry, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK.
Background: Attention-deficit/hyperactivity disorder (ADHD) is commonly attributed to neuro-cognitive deficits of genetic and/or prenatal/perinatal environmental origins. Sonuga-Barke proposed an alternative formulation, suggesting that ADHD behaviors are functional expressions of delay aversion-a strong motivational disposition to avoid or escape negative affective states evoked by delay. It is hypothesized that the strength of this disposition, though neuro-biologically rooted, is exacerbated by early negative social interactions during waiting-related encounters.
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