Folia neuropathologica最新文献

Parkinson's disease (PD) is a chronic neuronal loss of dopamine and drugs used for its management has several limitations. The present report determines the effect of exercise on mitochondrial autophagy against PD. Parkinson's disease was induced by 15 doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 30 mg/kg, i.p.) for 3 weeks, on five consecutive days in a week. Exposure of exercise was provided for 40 min for a period of 2 weeks after PD confirmation. Assessment of behaviour was performed to evaluate the effect of exercise on motor function and cognitive function in PD rats. Levels of reactive oxygen species (ROS) and inflammatory cytokines were assessed in PD rats using enzyme linked immunosorbent assay (ELISA). Expression of myocyte-specific enhancer factor 2D (MEF2D) and NADH dehydrogenase 6 (ND6) was estimated in PD rats. Exposure to exercise ameliorates the altered motor function and cognitive function in PD rats. There was a reduction in ROS and cytokine levels in the brain tissue of the exercise group compared to the negative control group. Exercise ameliorates the altered expression of apoptotic proteins and mRNA expression of MEF2D and ND6 in the brain tissue of MPTP induced PD rats. In conclusion, data of study reveal that exercise protects the mitochondrial autophagy in PD rats by reducing inflammatory cytokines and oxidative stress.

Alzheimer's disease (AD), also known as senile dementia, is a degenerative disease of the central nervous system and is characterized by insidious onset and a chronic progressive course. It is the most common type of senile dementia. Studies have proved that the deposition of amyloid b (Ab) in the brain is one of the initiating factors correlated to the pathology of AD, and it acts as one of the critical factors leading to the onset of AD. A large number of long-term studies have shown that Ab may be a therapeutic target for a breakthrough in the treatment of AD. This review elucidates the important role of Ab in the development of AD, current research on the role of Ab in AD pathogenesis, and treatment of AD by targeting Ab.

Introduction: Acute ischemic stroke (AIS) is a disease with high morbidity and mortality in the clinic. The current experiments aimed to study the effects of UCA1 interfering miR-18a-5p on cerebral ischemia-reperfusion (CI/R).

Material and methods: For rat models undergoing middle cerebral artery infarction (MCAO) surgery, the expression of UCA1 and miR-18a-5p was evaluated by qRT-PCR, and underlying function was identified by detecting infarct size, neurological scores, and inflammation. Luciferase report was applied to verify the relationship between UCA1 and miR-18a-5p. In the cell models, the impacts of UCA1 and miR-18a-5p were validated by CCK-8 assay, flow cytometry analysis, and ELISA. In patients with AIS, Pearson correlation was carried out to unveil the association between UCA1 and miR-18a-5p.

Results: The expression of UCA1 was at high levels and miR-18a-5p was at low levels in AIS patients. UCA1 knockdown showed a protective role in infarct size, neurofunction, and inflammation via binding miR-18a-5p. MiR-18a-5p participated in the regulation of UCA1 on cell viability, cell apoptosis, lactate dehydrogenase (LDH) levels, and inflammation. In patients with AIS, overexpression of UCA1 and underexpression of miR-18a-5p had a reverse correlation.

Conclusions: Elimination of UCA1 was favourable to the recovery of the rat model and cells from CI/R damage by efficaciously sponging miR-18a-5p.

Introduction: Since December 2019, coronavirus 2019 (COVID-19) has rapidly spread to become a global pandemic, exerting a great pressure on medical staff worldwide. This study aimed to observe whether COVID-19 influenced the diagnosis and treatment of ischemic stroke (IS).

Material and methods: This study retrospectively analysed the clinical data (number of emergencies, time from onset to treatment, and door-to-needle time [DNT]) of patients with acute IS (AIS) treated in our hospital within six months of the first case of COVID-19 reported in the city; the derived data were then compared with the situation of patients during the same period in 2019.

Results: The results showed that the number of medical visits during the period of COVID-19 decreased by 44.3%, and the median time from the onset of IS to emergency treatment was 35 min longer than that during the same period in 2019. The median time from entering the emergency department to the completion of cranial computerized tomography was 8 min shorter than during the same period in 2019, and the median time of DNT was relatively shorter than that during the same period in 2019.

Conclusions: The pandemic situation of COVID-19 significantly reduced the number of patients with AIS and prolonged the travel time to the hospital whereas most of the stroke treatment services were maintained.

Introduction: Osteopontin (OPN) is involved in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). The aim of this study was to investigate the expression of OPN in spinal cords of mice in the successive phases of EAE, to compare it with the density of inflammatory cells, oligodendrocytes and with the expression of interleukin (IL)-17A and to assess the effect of anti-α4β1 integrin (VLA-4) treatment.

Material and methods: Experimental autoimmune encephalomyelitis (EAE) mice were injected with anti-VLA-4 antibodies or, as treatment control, with immunoglobulin G (IgG). Spinal cords were sectioned and immunostained for OPN, CD45 (overall leukocytes), CD3 (T cells), Iba1 (activated macrophages/microglia), IL-17A, and CNP1 (oligodendrocytes). Microscopic images were analysed and the percentage of immunopositive areas encompassing the whole spinal cord cross-sectional area were assessed in images for each antigen.

Results: Osteopontin was expressed by inflammatory cells and by a minority of neurons and blood vessels. Most of the studied parameters followed the temporal pattern of clinical scores: increase in the peak phase and decrease in the chronic phase. Only OPN and IL-17A remained at a high level in the chronic phase, while CNP1 expression gradually decreased in the successive phases. Anti-VLA-4 treatment lowered the expression of the studied antigens in the peak and chronic phases with the exception of oligodendrocyte marker CNP1 which in both phases showed an increased expression.

Conclusions: Involvement of OPN is particularly significant in advanced EAE. Anti-VLA-4 treatment not only inhibits migration of myelin-reactive T cells, but also downregulates OPN and inhibits loss of oligodendrocytes.

Introduction: To observe the 24-h ambulatory blood pressure characteristics of patients with acute ischemic stroke and explore the correlation between blood pressure variability and strictly deep cerebral microbleeds (CMBs).

Material and methods: A convenient sampling method was used to enrol 131 patients with acute ischemic stroke in the Department of Neurology between April 2021 and May 2022. Hospitalised patients with acute ischemic stroke were assessed retrospectively; their ambulatory blood pressure was monitored continuously for 24 h, and the relevant parameters were recorded. Magnetic susceptibility-weighted imaging was used to divide the CMBs into a strictly deep CMB group ( n = 24) and a non-CMB group ( n = 107) according to the location of the CMBs. A logistic regression analysis was performed to determine the independent correlation between the 24-h ambulatory blood pressure parameters and strictly deep CMBs. The receiver operating characteristic (ROC) was further used to analyse the predictive value of the ambulatory blood pressure parameters for strictly deep CMBs in patients with acute ischemic stroke.

Results: The results showed that the night systolic blood pressure standard deviation and the night diastolic blood pressure standard deviation (NDBP-SD) in the strictly deep CMB group were higher than those in the non-CMB group ( p < 0.05). The multiple logistic regression analysis indicated that the NDBP-SD (odds ratio [OR] = 1.205, 95% confidence interval [CI]: 1.011-1.436, p = 0.038) was an independent risk factor for strictly deep CMBs in patients. The ROC curve analysis revealed that the area under the curve value of the NDBP-SD was 0.682, and the intercept was 7.81. When NDBP-SD is ≥ 7.81, the occurrence of strictly deep CMBs is closely related (OR = 3.872, 95% CI: 1.347-11.125, p = 0.012).

Conclusions: The NDBP-SD is an independent risk factor for strictly deep CMBs in patients with acute ischemic stroke. When NDBP-SD is > 7.81, it may promote the production of strictly deep CMBs.