scholarly journals Activation of pro-apoptotic cells, reactive astrogliosis and hyperphosphorylation of tau protein in trimethyltin-induced hippocampal injury in rats

2020 ◽  
Vol 9 (2) ◽  
pp. 1782-1788
Author(s):  
A.A. Okesina ◽  
M.S. Ajao ◽  
M.O. Buhari ◽  
A.M. Afodun ◽  
K.B. Okesina ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Tau Protein ◽  
Genetic Factors ◽  
Disease Model ◽  
Amyloid Plaques ◽  
Control Group ◽  
Neural Cells ◽  
Reactive Astrogliosis ◽  
Parkinson’S Diseases ◽  
Male Wistar Rats

Neurodegenerative diseases cause neural cells to lose both the functional and sensory abilities as a result of genetic factors, proteopathies and mitochondrial dysfunction. Neurodegeneration forms the basis of most neurodegenerative disorders for example Alzheimer’s disease, Huntington’s diseases, and Parkinson’s diseases. The mechanism that underlines the process of neurodegeneration is not well understood. Understanding the process and mechanism involved in neurodegeneration might offer a better therapeutic approach to positively manage cases of neurodegenerative diseases. Therefore, this study’s target was to create an animal model to study neurodegeneration. Sixteen adult male Wistar rats were used in the study and divided into two groups. Control (0.2 mL of normal saline (NS)), and trimethyltin-treated (TMT, 8 mg/kg stat dose only). These animals underwent perfusion with 4% paraformaldehyde, brain excision and analysis of p53 antigen, GFAP and Bielshowsky on these tissues. The results showed that animals in the control group showed presence of activated p53 antigen, reactive astrogliosis, neurofibrillary tangles, and amyloid plaques within the cytoplasm of the hippocampal cells. Cornus Ammonis (CA2) and (CA3) showed more of the trimethylrtin injury than CA1 and CA4. This study thus revealed that, intra-peritoneal administration of single dose of 8mg/kg of trimethyltin can offer an attractive disease model to study some neurodegenerative diseases. Keywords: p53 antigen, Bielshowsky, Glia fibrillary acidic protein, Trimethyltin, Hippocampus,

An experimental model of neurodegenerative disease based on porcine hemagglutinating encephalomyelitis virus-related lysosomal abnormalities

2020 ◽  
Author(s):  
Yungang Lan ◽  
Zi Li ◽  
Zhenzhen Wang ◽  
Xinran Wang ◽  
Gaili Wang ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Neuronal Ceroid Lipofuscinosis ◽  
Disease Model ◽  
Experimental Models ◽  
Neural Cells ◽  
Specific Mechanism ◽  
Encephalomyelitis Virus ◽  
Infected Cells ◽  
First Time ◽  
Porcine Hemagglutinating Encephalomyelitis Virus

Abstract Advances in experimental models for neurodegenerative diseases have enhanced the understanding of its molecular pathogenesis and begun to revealed promising therapeutic avenues. Lysosomes are involved in pathogenesis of a variety of neurodegenerative diseases and play a large role in neurodegenerative disorders caused by virus infection. However, whether virus-infected cells or animals can be used as experimental models of neurodegeneration in humans based on virus-related lysosomal dysfunction remain unclear. Porcine hemagglutinating encephalomyelitis virus (PHEV) displays neurotropism in mice and neural cells are its targets for viral progression. PHEV infection may be a risk factor for neurodegenerative diseases. Our findings demonstrated for the first time that PHEV infection can lead to lysosome disorders and showed that the specific mechanism of lysosome dysfunction is related to PGRN expression deficiency and indicated similar pathogenesis compared to human neurodegenerative diseases such as neuronal ceroid lipofuscinosis (NCL) and frontotemporal lobar degeneration (FTLD) upon PHEV infection. Trehalose can also increase progranulin (PGRN) expression and rescue abnormalities in lysosomal structure in PHEV-infected cells. In conclusion, these results suggest that PHEV may serve as a disease model for studying the pathogenic mechanisms and prevention of other degenerative diseases.

scholarly journals Unlocking the Complexity of Mitochondrial DNA: A Key to Understanding Neurodegenerative Disease Caused by Injury

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3460
Author(s):  
Larry N. Singh ◽  
Shih-Han Kao ◽  
Douglas C. Wallace
Keyword(s):  
Mitochondrial Dna ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disease ◽  
Genetic Factors ◽  
Mitochondrial Genetics ◽  
Dna Variation ◽  
Parkinson’S Diseases ◽  
And Function ◽  
The Impact

Neurodegenerative disorders that are triggered by injury typically have variable and unpredictable outcomes due to the complex and multifactorial cascade of events following the injury and during recovery. Hence, several factors beyond the initial injury likely contribute to the disease progression and pathology, and among these are genetic factors. Genetics is a recognized factor in determining the outcome of common neurodegenerative diseases. The role of mitochondrial genetics and function in traditional neurodegenerative diseases, such as Alzheimer’s and Parkinson’s diseases, is well-established. Much less is known about mitochondrial genetics, however, regarding neurodegenerative diseases that result from injuries such as traumatic brain injury and ischaemic stroke. We discuss the potential role of mitochondrial DNA genetics in the progression and outcome of injury-related neurodegenerative diseases. We present a guide for understanding mitochondrial genetic variation, along with the nuances of quantifying mitochondrial DNA variation. Evidence supporting a role for mitochondrial DNA as a risk factor for neurodegenerative disease is also reviewed and examined. Further research into the impact of mitochondrial DNA on neurodegenerative disease resulting from injury will likely offer key insights into the genetic factors that determine the outcome of these diseases together with potential targets for treatment.

scholarly journals Synergetic Treatment of Ascorbic Acid and Nicotine Ameliorates Aluminium Induced Neurotoxicity in the Prefrontal Cortex of Wistar Rat

2021 ◽  
Vol 5 (2) ◽  
pp. 282-288
Author(s):  
Taiwo A. Abayomi
Keyword(s):  
Ascorbic Acid ◽  
Body Weight ◽  
Prefrontal Cortex ◽  
Wistar Rats ◽  
Amyloid Plaques ◽  
Wistar Rat ◽  
Aluminium Chloride ◽  
Control Group ◽  
Male Wistar Rats

Background: Though the neuroprotective roles of ascorbic acid are well established, the therapeutic role of nicotine in various neurological disorders is attracting increasing attention. This study evaluated the putative ameliorative role of the synergetic treatment of nicotine and ascorbic acid against neurodegenerative consequences associated with free radical species and amyloid plaques generation in adult male Wistar rats Methods: A total of 35 Wistar rats were distributed into five groups labeled A-E. Group A served as the control group; animals in group B were treated with 100mg/kg body weight of aluminium chloride (AlCl3) for 21 days. Group C animals were treated with 100mg/kg body weight of aluminium chloride for 21 days and post-treated with 14mg/kg body weight of nicotine for 21 days. Group D was treated with 100mg/kg body weight of aluminium chloride for 21 days and post-treated with 100mg/kg bodyweight of ascorbic acid for 21 days. Group E animals were treated with 100mg/kg body weight of aluminium chloride for 21 days and post-treated with 100mg/kg bodyweight of ascorbic acid and 14mg/kg body weight of nicotine. On completion of treatments, the prefrontal cortex was excised and processed for biochemical and histochemical examinations. Results: Oxidative stress was evident from the diminished level of catalase and glutathione per oxidase and elevated lipid peroxidation levels in animals administered with aluminium in addition to the presence of amyloid plaques in these animals. However, synergetic administration of ascorbic acid and nicotine attenuated these oxidative and histochemical perturbations induced by aluminium. Conclusion: Synergetic treatment with ascorbic acid and nicotine provided better ameliorative potential against aluminium-induced neurotoxicity compared to either ascorbic acid or nicotine treatments alone

scholarly journals Neurodegenerative changes in the brainstem and olfactory bulb in people older than 50 years old: a descriptive study

2015 ◽  
Vol 73 (7) ◽  
pp. 569-577 ◽  
Author(s):  
Francine Hehn de Oliveira ◽  
Edson Rodrigues Neto ◽  
Mariana Kumaira Fonseca ◽  
André Silvestre Reitz da Costa ◽  
Marcio Aloisio Bezerra Cavalcanti Rockenbach ◽  
...  
Keyword(s):  
Life Expectancy ◽  
Olfactory Bulb ◽  
Neurodegenerative Diseases ◽  
Tau Protein ◽  
Final Diagnosis ◽  
Descriptive Study ◽  
Limbic Cortex ◽  
Olfactory Bulbs ◽  
Protein Deposits ◽  
Parkinson’S Diseases

With the increase in life expectancy in Brazil, concerns have grown about the most prevalent diseases in elderly people. Among these diseases are neurodegenerative diseases, such as Alzheimer’s and Parkinson’s diseases. Protein deposits related to the development of these diseases can pre-date the symptomatic phases by years. The tau protein is particularly interesting: it might be found in the brainstem and olfactory bulb long before it reaches the limbic cortex, at which point symptoms occur. Of the 14 brains collected in this study, the tau protein was found in the brainstems of 10 (71.42%) and in olfactory bulbs of 3 out 11. Of the 7 individuals who had a final diagnosis of Alzheimer’s disease (AD), 6 presented tau deposits in some region of the brainstem. Our data support the idea of the presence of tau protein in the brainstem and olfactory bulb in the earliest stages of AD.

Chronic immobilization stress induces anxiety-related behaviors and affects brain essential minerals in male rats

2020 ◽  
pp. 1-8
Author(s):  
Zafer Sahin ◽  
Alpaslan Ozkurkculer ◽  
Omer Faruk Kalkan ◽  
Ahmet Ozkaya ◽  
Aynur Koc ◽  
...  
Keyword(s):  
Immobilization Stress ◽  
Central Area ◽  
Essential Elements ◽  
Male Rats ◽  
Control Group ◽  
Male Wistar Rats ◽  
Swimming Test ◽  
The Brain ◽  
Center Area ◽  
Chronic Immobilization Stress

Abstract. Alterations of essential elements in the brain are associated with the pathophysiology of many neuropsychiatric disorders. It is known that chronic/overwhelming stress may cause some anxiety and/or depression. We aimed to investigate the effects of two different chronic immobilization stress protocols on anxiety-related behaviors and brain minerals. Adult male Wistar rats were divided into 3 groups as follows ( n = 10/group): control, immobilization stress-1 (45 minutes daily for 7-day) and immobilization stress-2 (45 minutes twice a day for 7-day). Stress-related behaviors were evaluated by open field test and forced swimming test. In the immobilization stress-1 and immobilization stress-2 groups, percentage of time spent in the central area (6.38 ± 0.41% and 6.28 ± 1.03% respectively, p < 0.05) and rearing frequency (2.75 ± 0.41 and 3.85 ± 0.46, p < 0.01 and p < 0.05, respectively) were lower, latency to center area (49.11 ± 5.87 s and 44.92 ± 8.04 s, p < 0.01 and p < 0.01, respectively), were higher than the control group (8.65 ± 0.49%, 5.37 ± 0.44 and 15.3 ± 3.32 s, respectively). In the immobilization stress-1 group, zinc (12.65 ± 0.1 ppm, p < 0.001), magnesium (170.4 ± 1.7 ppm, p < 0.005) and phosphate (2.76 ± 0.1 ppm, p < 0.05) levels were lower than the control group (13.87 ± 0.16 ppm, 179.31 ± 1.87 ppm and 3.11 ± 0.06 ppm, respectively). In the immobilization stress-2 group, magnesium (171.56 ± 1.87 ppm, p < 0.05), phosphate (2.44 ± 0.07 ppm, p < 0.001) levels were lower, and manganese (373.68 ± 5.76 ppb, p < 0.001) and copper (2.79 ± 0.15 ppm, p < 0.05) levels were higher than the control group (179.31 ± 1.87 ppm, 3.11 ± 0.06 ppm, 327.25 ± 8.35 ppb and 2.45 ± 0.05 ppm, respectively). Our results indicated that 7-day chronic immobilization stress increased anxiety-related behaviors in both stress groups. Zinc, magnesium, phosphate, copper and manganese levels were affected in the brain.

Dietary Calcium Supplementation Suppresses Bone Formation in Magnesium-Deficient Rats

2006 ◽  
Vol 76 (3) ◽  
pp. 111-116 ◽  
Author(s):  
Hiroshi Matsuzaki ◽  
Misao Miwa
Keyword(s):  
Bone Formation ◽  
Calcium Supplementation ◽  
Control Diet ◽  
Formation Rate ◽  
Dietary Calcium ◽  
Mineral Apposition Rate ◽  
Control Group ◽  
Deficient Diet ◽  
Bone Formation Rate ◽  
Male Wistar Rats

The purpose of this study was to clarify the effects of dietary calcium (Ca) supplementation on bone metabolism of magnesium (Mg)-deficient rats. Male Wistar rats were randomized by weight into three groups, and fed a control diet (control group), a Mg-deficient diet (Mg- group) or a Mg-deficient diet having twice the control Ca concentrations (Mg-2Ca group) for 14 days. Trabecular bone volume was significantly lower in the Mg - and Mg-2Ca groups than in the control group. Trabecular number was also significantly lower in the Mg - and Mg-2Ca groups than in the control group. Mineralizing bone surface, mineral apposition rate (MAR), and surface referent bone formation rate (BFR/BS) were significantly lower in the Mg - and Mg-2Ca groups than in the control group. Furthermore, MAR and BFR/BS were significantly lower in the Mg-2Ca group than in the Mg - group. These results suggest that dietary Ca supplementation suppresses bone formation in Mg-deficient rats.

Berat Badan, Panjang Badan dan Faktor Genetik sebagai Prediktor Terjadinya Stunted pada Anak Sekolah

2017 ◽  
Vol 19 (2) ◽  
pp. 95
Author(s):  
Hetriana Leksananingsih ◽  
Slamet Iskandar ◽  
Tri Siswati
Keyword(s):  
Birth Weight ◽  
Nutritional Status ◽  
School Children ◽  
Genetic Factors ◽  
Control Group ◽  
Case Group ◽  
Normal Birth Weight ◽  
Chi Square ◽  
Normal Birth ◽  
Chi Square Test

Background: Riskesdas in 2013 showed that Yogyakarta (DIY) had a prevalence of stunted new kid in school is less than the national average, which is 14.9% (MOH, 2013). Stunted or short, is a linear growth retardation has been widely used as an indicator to measure the nutritional status of individuals and community groups. Stunted can be influenced by several factors: birth weight, birth length match and genetic factors. Objective: To determine the weight, length of low birth weight and genetic factors as predictors of the occurrence of stunted on elementary school children. Methods: The study was a case control analytic. Research sites in SD Muhammadiyah Ngijon 1 Subdistrict Moyudan. The study was conducted in May and June 2015. The subjects were school children grade 1 to grade 5 the number of cases as many as 47 children and 94 control children. With the inclusion criteria of research subjects willing to become respondents, was present at the time of the study, they have a father and mother, and exclusion criteria have no data BB and PB birth, can not stand upright. The research variables are BBL, PBL, genetic factors and TB / U at this time. Data were analyzed by chi-square test and Odd Ratio (OR) calculation. Results: In case group as much as 91.5% of normal birth weight and length of 80.9% of normal birth weight, most of the height of a normal mother and father as many as 85.1%. In the control group as much as 78.7% of normal birth weight and 61.7% were born normal body length, height mostly normal mom and dad that 96.7% of women and 90.4% normal normal father. Statistical test result is no significant correlation between height mothers with stunted incidence in school children, and the results of chi-square test P = 0.026 with value Odd Ratio (OR) of 3.9 and a range of values from 1.091 to 14.214 Cl95%. Conclusion: High maternal body of mothers can be used as predictors of the occurrence of stunted school children and mothers with stunted nutritional status have 3.9 times the risk of having children with stunted nutritional status.

Pengaruh Profilaksis Ekstrak Ubi Jalar Ungu (Ipomoea batatas L.) terhadap Kadar Malondialdehida Hepar Tikus Putih (Rattus norvegicus) Jantan Galur Wistar yang Diinduksi Karagenan

2018 ◽  
Vol 15 (2) ◽  
pp. 146
Author(s):  
BRILIAN DINANTI ◽  
FITRI HANDAJANI
Keyword(s):  
Sweet Potato ◽  
Ipomoea Batatas ◽  
Wistar Rats ◽  
Group Method ◽  
Control Group ◽  
Intraplantar Injection ◽  
Significant Difference ◽  
Male Wistar Rats ◽  
Potato Extract ◽  
Purple Sweet Potato

<p>Liver is an organ with complex metabolism. When the liver is inflamed, cellular immunity will defend against inflammatory agents by stimulating immune cells to produce reactive oxygen species (ROS). Excessive ROS accumulation cause oxydative stress with increased  liver malondialdehyde (MDA) level. Some researches showed that purple sweet potato contain flavonoids (anthocyanins) that functioned as antioxydants. This study aimed to show the prophylactic effect of purple sweet potato extract to the liver MDA level of male Wistar rats induced by carrageenan.</p><p>This study used post-only control group method using 18 male Wistar rats divided into 3 groups: group of rats without treatment, group of rats induced by 0,1 ml of 1% carrageenan by intraplantar injection on day-8, and group of rats given with 872 mg/kgBW of purple sweet potato extract for 7 days and induced by 0,1 ml of 1% carrageenan. In the end of the study, the liver MDA levels were measured by Thio-Barbituric Acid method on each groups.</p><p>The results of One-Way ANOVA test showed there was no significant difference (p = 0,290) between group of rats without treatment (<em>x̅</em>= 207,50) and group of rats induced by carrageenan (<em>x̅</em>=233,17). Then, there is no significant difference (p = 0.978) between group of rats induced by carrageenan and group of rats given with prophylactic purple sweet potato extract and induced by carrageenan (<em>x̅</em>= 232,50).</p><p>The conclusion of this study is giving intraplantar injection of carrageenan can increase liver MDA level insignificantly and giving prophylactic purple sweet potato extract has an effect to decrease the liver MDA level of rats induced by carragenan insignificantly because it contains anthocyanins as antioxidants.</p><p> </p><strong>Keywords: </strong>Liver, <em>Ipomoea batatas</em> L., Malondialdehyde, Anthocyanins

Mechanism Involved in Fortification by Berberine in CDDP-Induced Nephrotoxicity

2020 ◽  
Vol 13 (4) ◽  
pp. 342-352 ◽  
Author(s):  
Vipin K. Verma ◽  
Salma Malik ◽  
Ekta Mutneja ◽  
Anil K. Sahu ◽  
Kumari Rupashi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Tissue ◽  
Isoquinoline Alkaloid ◽  
Experimental Models ◽  
Beclin 1 ◽  
Control Treatment ◽  
Control Group ◽  
Treatment Groups ◽  
Single Intraperitoneal Injection ◽  
Male Wistar Rats

Background: The activation of Nrf2/HO-1 pathway has been shown to protect against cisplatin- induced nephrotoxicity by reducing oxidative stress. Berberine (Ber), an isoquinoline alkaloid, has demonstrated antioxidant, anti-inflammatory and anti-apoptotic activities in various experimental models. Aim: To check the effect of Ber on cisplatin-induced nephrotoxicity and to explore the involved mechanism. Methods: Adult male Wistar rats were divided into 6 groups: Normal, cisplatin-control, treatment groups and per se group. Normal saline and Ber (20, 40 and 80 mg/kg; p.o.) was administered to rats for 10 days. A single intraperitoneal injection of cisplatin (8 mg/kg) was injected on 7th day to induced nephrotoxicity. On 10th day, rats were sacrificed, the kidney was removed and stored for the estimation of various parameters. Results: As compared to cisplatin-control group, Ber pretreatment improved renal function system and preserved renal architecture. It also diminished oxidative stress by upregulating the expression of Nrf2/HO-1 proteins. In addition, Ber attenuated the cisplatin mediated inflammation and apoptosis. Furthermore, it also reduced the phosphorylation of p38/JNK and PARP/Beclin-1 expression in the kidney. Conclusion: Ber attenuated renal injury by activating Nrf2/HO-1 and inhibiting JNK/p38MAPKs/ PARP/Beclin-1 expression which prevented oxidative stress, inflammation, apoptosis and autophagy in renal tissue.

scholarly journals Emerging hiPSC Models for Drug Discovery in Neurodegenerative Diseases

2021 ◽  
Vol 22 (15) ◽  
pp. 8196
Author(s):  
Dorit Trudler ◽  
Swagata Ghatak ◽  
Stuart A. Lipton
Keyword(s):  
Drug Discovery ◽  
Animal Models ◽  
Neurodegenerative Diseases ◽  
Disease Modeling ◽  
Induced Pluripotent Stem Cell ◽  
Neural Function ◽  
Neural Cells ◽  
Human Samples ◽  
Healthy Donors ◽  
Induced Pluripotent

Neurodegenerative diseases affect millions of people worldwide and are characterized by the chronic and progressive deterioration of neural function. Neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD), represent a huge social and economic burden due to increasing prevalence in our aging society, severity of symptoms, and lack of effective disease-modifying therapies. This lack of effective treatments is partly due to a lack of reliable models. Modeling neurodegenerative diseases is difficult because of poor access to human samples (restricted in general to postmortem tissue) and limited knowledge of disease mechanisms in a human context. Animal models play an instrumental role in understanding these diseases but fail to comprehensively represent the full extent of disease due to critical differences between humans and other mammals. The advent of human-induced pluripotent stem cell (hiPSC) technology presents an advantageous system that complements animal models of neurodegenerative diseases. Coupled with advances in gene-editing technologies, hiPSC-derived neural cells from patients and healthy donors now allow disease modeling using human samples that can be used for drug discovery.

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