جستجوی مقالات مرتبط با کلیدواژه « neurodegenerative diseases » در نشریات گروه « پزشکی »

Propylene glycol (PG) is frequently used as a solvent for various medications. However, there is substantial evidence of Propylene glycol toxicity, such as depression, agitation, and seizures, particularly when used in combination with other drugs. Here, we aimed to study the effect of Propylene glycol administration in combination with amyloid β₁₋₄₀ injection on hippocampal neurons.

Thirty-six male Wistar rats were randomly divided into four groups: sham, amyloid β₁₋₄₀ injection group, Propylene glycol group, and amyloid β₁₋₄₀ + Propylene glycol group. Alternation behavior, number of neurons in the hippocampus, lipid peroxidation markers, and superoxide dismutase levels were analyzed in all rats.

When Propylene glycol was co-administered with amyloid β₁₋₄₀, a notable reduction in the mean neuronal count was observed in the CA1, CA3, and DG regions compared with the amyloid β₁₋₄₀ only injected animals (P < 0.05). Furthermore, Propylene glycol induced an increase in lipid peroxidation markers (10.78 ± 0.4) and a decrease in antioxidant content (2.8 ± 0.17) when administered with amyloid β₁₋₄₀, compared to the animals that received only amyloid β₁₋₄₀ (P < 0.05). A similar pattern was found in alternation behavior compared with the group with amyloid β₁₋₄₀ injection (P < 0.001).

 Propylene glycol could produce excessive neurotoxicity in regions of the hippocampus when co-administered with amyloid β₁₋₄₀. It likely increases lipid peroxidation and reduces superoxide dismutase in the rat brain. The use of different agents as a vehicle should be considered, especially in the elderly.

Alzheimer’s disease (AD) is a neurodegenerative condition characterized by gradual cognitive impairment, including loss of synapses and nerve cells involved in learning, memory, and habit formation processes. Bone Marrow Mesenchymal Stem Cells (BM-MSCs) are multipotent cells. Because of their self-renewable, differentiation, and immunomodulatory capabilities, they are commonly used to treat many disorders. Hence, the current study intends to examine the effect of BM-MSCs transplantation on Aluminum chloride (AlCl3)-induced cognitive problems, an experimental model resembling AD’s hallmarks in rats. The study was conducted in 2022 at The Biomedical Laboratory Faculty of Medicine, Andalas University, Indonesia. Adult male Wistar rats (three groups: negative control; no intervention+treatment with PBS; positive control: AlCl3+treatment with aqua dest; AlCl3+BM-MSCs: AlCl3+treatment with BM-MSCs, n=5 each) were treated daily with AlCl3 orally for five days. Stem cells were intraperitoneally injected into rats at a dose of 1x106 cells/rat. The same quantity of phosphate-buffered saline was given to the control group. One month after stem cell injection, the rat brain tissue was removed and placed in the film bottles that had been created. The expression of neural progenitor cell markers, including nestin and sex-determining Y-box 2 (SOX-2), was analyzed using real-time polymerase chain reaction (RT-PCR). Rats’ cognitive and functional memory were examined using Y-maze. Data were analyzed using SPSS software (version 26.0) with a one-way analysis of variance (ANOVA) test. The gene expression of nestin (29.74±0.42), SOX-2 (31.44±0.67), and percent alternation of Y-maze (67.04±2.28) increased in the AlCl3+BM-MSCs group compared to that in the positive control group. RT-PCR analysis indicated that nestin (P<0.001) and SOX-2 (P<0.001) were significantly enhanced in the AlCl3+BM-MSCs group compared to the positive control group. This group also indicated an increased percent alternation of Y-maze (P<0.001) in the AlCl3+BM-MSCs group compared to the positive control group.  Due to its potential effects on cell therapy, BM-MSCs were found effective in a rat model of AD on the impairment of the rats’ behavior and increased expression of neural progenitor cell markers.

Cognitive disorders, characterized by transient stages and potential Alzheimer's disease, are influenced by changes in iron deposits in the brain. These changes can lead to toxicity and neuron death. Quantitative susceptibility mapping is used to accurately represent these changes, allowing for a more accurate evaluation of the time window of each cognitive disorder stage and the need for targeted treatment. The Alzheimer's Disease Neuroimaging Initiative research database was used to download the data and eight healthy participants and twenty-one participants with cognitive disorders based on MMSE cognitive test scores in 5 groups of cognitively normal, Subjective Memory Concern , Early Mild Cognitive Impairment, Late Mild Cognitive Impairment and Alzheimer's disease were included in this study. Quantitative Susceptibility Mapping processing was performed using the SEPIA toolbox in MATLAB, and segmentation was performed using FSL software. Finally, statistical analyzes were performed using SPSS V26 software. Statistically significant changes were observed in the QSM values of the right thalamus (p-value = 0.043) in the LMCI group and the right hippocampal nucleus (p-value = 0.050) in the control group. After one year, the right hippocampal nucleus shows increased iron accumulation in healthy individuals, suggesting that the nucleus is susceptible to the highest rate of iron deposition in healthy individuals. Based on this result, the hypothesis that iron deposits are the cause of the unknown cause-and-effect relationship between iron deposits and Alzheimer's disease may be confirmed.

Protein aggregation is a complex process that plays a key role in the development of various diseases, including neurodegenerative disorders, metabolic conditions, and systemic amyloidoses. This brief review summarizes the current understanding of the mechanisms behind protein aggregation, its impact on disease progression, and potential treatment approaches. We extensively researched recent influential publications, critically evaluated relevant articles, and synthesized key concepts, emerging trends, and promising research areas. Genetic mutations, environmental stress, and aging all contribute to the misfolding and aggregation of proteins. The aggregation process is influenced by thermodynamic and kinetic factors, involving stages such as nucleation, elongation, and the formation of aggregate structures. Biological systems, including molecular chaperones, the ubiquitin-proteasome pathway, and autophagy, play crucial roles in preventing and managing protein aggregates. Pathological protein aggregation is associated with diseases such as Alzheimer's, Parkinson's, prion diseases, cataracts, type II diabetes, and systemic amyloidoses. The review also emphasizes the potential of therapeutic strategies, such as small molecule inhibitors, immunotherapy, modulation of proteostasis pathways, nanotechnology, and gene therapy, in addressing these debilitating diseases. A comprehensive understanding of protein aggregation mechanisms and the development of effective therapeutic interventions offer hope in the fight against these diseases. This review provides current insights and recommends future research directions, highlighting the significant implications for human health and treatment innovation.

Alzheimer's Disease (AD) is one of the most prevalent chronic neurodegenerative disorders. The present study aims to better understand the mechanism by which Citrus aurantium (C. aurantium) and Lavandula angustifolia (L. angustifolia) hydro–alcoholic extracts were used to treat AD and anti –oxidant issues in a laboratory model.

15 male Wistar rats, weighing 250±20 gr, aged 6–8 weeks, were used. Amyloids in the brain were found and identified using the shuttle box and Congo red test. ELISA testing for norepinephrine and serotonin, Superoxide Dismutase (SOD), Malondialdehyde (MDA), and Real–time PCR for expression of the APP and GLT1 genes were done.

The shuttle box test demonstrated that AD produces behavioral harm, since it significantly reduces passive avoidance learning. The Congo red test revealed that the AD models had much more amyloid beta in their brain tissue than the control. Norepinephrine levels were also decreased by using both extracts in test group. Treatment with both extracts led to a substantial rise in SOD activity and fall in MDA concentration.

The gene expression data indicated that the relative expression of the APP and GLT1 genes was shown to be lower in the groups treated with both extracts. C. aurantium and L. angustifolia may therefore offer a multi–target treatment strategy for AD, which calls for more research in this area.

One of the most challenging problems of the current treatments of neurodegenerative diseases is related to the permeation and access of most therapeutic agents to the central nervous system (CNS), prevented by the blood-brain barrier (BBB). Recently, intranasal (IN) delivery has opened new prospects because it directly delivers drugs for neurological diseases into the brain via the olfactory route. Recently, PLGA-based nanocarriers have attracted a lot of interest for IN delivery of drugs. This review gathered clear and concise statements of the recent progress of the various developed PLGA-based nanocarriers for IN drug delivery in brain diseases including Alzheimer’s, Parkinson’s, brain tumors, ischemia, epilepsy, depression, and schizophrenia. Subsequently, future perspectives and challenges of PLGA-based IN administration are discussed briefly.

Neurodegenerative diseases are comprise a prominent class of neurological diseases. Generally, neurodegenerative diseases cannot be cured, and the available treatments can only regulate the symptoms or delay the disease progression. Among the several factors which could clarify the possible pathogenesis of neurodegenerative diseases, next to aging as the main risk, the dietary related diseases are the most important. Vegetable oils, which are composed of triacyclglycerols as the main components and several other components in a trace amount, are the main part of our diet. This review aims to study the effect of refined or unrefined vegetable oil consumption as a preventive or aiding strategy to slow or halt the progression of neurodegenerative diseases. In the refining process, owing to the chemical materials or severe temperatures of the refining process, removal of the desirable minor components is sometimes unavoidable and thus a worrisome issue affecting physical and neurological health.

Deep brain stimulation (DBS) is a surgically-based treatment for advanced Parkinson’s disease (PD) that has undergone technological developments. Artificial intelligence (AI) has been used successfully in many healthcare problems, including DBS. Indeed, DBS method is expected to change with the increasing growth of artificial intelligence, especially machine learning methods. So here we explore how AI can improve the results of DBS treatment.

Neurodegenerative diseases can make life difficult and lead to death in many cases. They also can be difficult, time-consuming, and costly to diagnose with enough accuracy/certainty. Artificial intelligence (AI) has shown promise in tackling some of the challenges present in medical imaging and is anticipated to become a crucial tool in health care applications in the near future. In particular, deep learning methods have displayed great performance in various subfields of image processing, including but not limited to image segmentation, image synthesis, and image reconstruction. In this paper, many state-of-the-art applications of deep learning models in image processing were reviewed.

Alzheimer’s disease (AD) is one of the most significant public health concerns and tremendous economic challenges. Studies conducted over the past decades show that exposure to radiofrequency electromagnetic fields (RF-EMFs) may relieve AD symptoms. 

To determine if exposure to RF-EMFs emitted by cellphones affect the risk of AD.

In this review, all relevant published articles reporting an association of cell phone use with AD were studied. We systematically searched international datasets to identify relevant studies. Finally, 33 studies were included in the review. Our review discusses the effects of RF-EMFs on the amyloid β (Aβ), oxidative stress, apoptosis, reactive oxygen species (ROS), neuronal death, and astrocyte responses. Moreover, the role of exposure parameters, including the type of exposure, its duration, and specific absorption rate (SAR), are discussed. 

Progressive factors of AD such as Aβ, myelin basic protein (MBP), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and neurofilament light polypeptide (NFL) were decreased. While tau protein showed no change, factors affecting brain activity such as glial fibrillary acidic protein (GFAP), mitogen-activated protein kinases (MAPKs), cerebral blood flow (CBF), brain temperature, and neuronal activity were increased.  

Exposure to low levels of RF-EMFs can reduce the risk of AD by increasing MAPK and GFAP and decreasing MBP. Considering the role of apoptosis in AD and the effect of RF-EMF on the progression of the process, this review indicates the positive effect of these exposures.

Evidence suggests that dysregulation in AMPA-type glutamate receptors (AMPA-Rs) has been associated with the pathogenesis of Alzheimer’s disease (AD), especially during its early phase. Hence, the present study was performed to elucidate the impact of resveratrol (RV) on hippocampal expression of AMPA-Rs in a rat model of AD.

A rat model of cognitive deficits was developed by a stereotactic intracerebroventricular infusion of lipopolysaccharide (LPS) in male Wistar rats (n=24). The LPS+RV30 group (n=12) received intraperitoneal injections of RV (30 mg/kg) at 30 min, 12 h, and 24 h before LPS injection. Meanwhile, the model (LPS) and sham (SO) groups only were treated with the vehicle solution (normal saline containing 1% ethanol). One day after the LPS infusion, the mRNA expressions of AMPA-Rs subunits (Gria1-4) were evaluated by RT–PCR. In addition, hippocampal levels of lipid peroxidation, superoxide dismutase, and nitric oxide were assessed. Seven days after the LPS challenge, the remaining animals (n=6, each group) were subjected to the Y-maze task, and the expression and localization of GluA1-containing AMPA-Rs in their hippocampi were investigated immunohistochemically.

Pretreatment with RV prevented LPS-induced cognitive dysfunction in rats and enhanced their working memory performance. Moreover, RV could moderately prevent oxidant-antioxidant imbalance in rats’ hippocampi. RT-PCR results revealed that the hippocampal mRNA expression of the Gria1 was significantly reduced, while the expressions of Gria2 and Gria3 were increased in LPS-challenged rats. RV significantly modulated the alteration in the Gria1 mRNA expression; however, it could not influence the Gria2 and Gria3 mRNA expressions. The immunohistochemical assessment showed a significantly reduced immunoreactivity for GluA1- containing AMPA-Rs in all hippocampal subfields of the LPS group, and RV could effectively ameliorate the alteration.

This study is the first to report that RV could modulate GluA1-containing AMPA-Rs dysregulation in a rat AD model.

In recent decades, it has been shown that the association between intestinal bacterial imbalance (dysbiosis) and various diseases such as type 2 diabetes can play a role in the development of Alzheimer's and Parkinson's diseases. In this study, the beneficial effects of intestinal microbiota glucagon-like peptide 1 (GLP-1) in cognitive disorders were investigated.

PubMed-Medline, Web of Science, and Scopus were searched to identify experimental studies based on the bacterial strains along with GLP-1 1 expression in preventing or reducing cognitive impairment. Of the 233 studies, six were eligible for inclusion, and the Systematic Review Centre for Laboratory animal Experimentation (SYRCLE) risk of bias tool was used to evaluate the risk of bias in individual studies.

The results showed that intestinal expression of GLP-1 1 could reduce the intestinal pathogenic genus such as Enterobacteriaceae and was obviously associated with a greater number of beneficial genera such as Lactobacillus and Akkermansia. Also, the neuroprotective effects of Clostridium butyricum with GLP-1 1 in a mice were approved. Therefore, the modulation of the intestinal microbiota, mediated by an increase in the intestinal GLP-1 1 level, consequently improved cognitive function.

In this review, we have indicated that the gut microbiota, by stimulating the expression of the intestinal hormones like GLP-1 1, and also with a beneficial effect in inhibiting some involved genes in inflammation, can declined the development of cognitive disorders.