Wyniki wyszukiwania

1

The role of dendritic cells in neurodegenerative diseases

100%

Iribarren P., Cui Y. H., Le Y., Wang J. M.

Archivum Immunologiae et Therapiae Experimentalis

|

2002

|

tom 50

|

nr 3

2

The role of advanced glycation end products in various types of neurodegenerative disease: a therapeutic approach

86%

Salahuddin P., Rabbani G., Khan R. H.

Cellular and Molecular Biology Letters

|

2014

|

tom 19

|

nr 3

Protein glycation is initiated by a nucleophilic addition reaction between the free amino group from a protein, lipid or nucleic acid and the carbonyl group of a reducing sugar. This reaction forms a reversible Schiff base, which rearranges over a period of days to produce ketoamine or Amadori products. The Amadori products undergo dehydration and rearrangements and develop a cross-link between adjacent proteins, giving rise to protein aggregation or advanced glycation end products (AGEs). A number of studies have shown that glycation induces the formation of the β-sheet structure in β-amyloid protein, α-synuclein, transthyretin (TTR), copper-zinc superoxide dismutase 1 (Cu, Zn-SOD-1), and prion protein. Aggregation of the β-sheet structure in each case creates fibrillar structures, respectively causing Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, familial amyloid polyneuropathy, and prion disease. It has been suggested that oligomeric species of glycated α-synuclein and prion are more toxic than fibrils. This review focuses on the pathway of AGE formation, the synthesis of different types of AGE, and the molecular mechanisms by which glycation causes various types of neurodegenerative disease. It discusses several new therapeutic approaches that have been applied to treat these devastating disorders, including the use of various synthetic and naturally occurring inhibitors. Modulation of the AGE-RAGE axis is now considered promising in the prevention of neurodegenerative diseases. Additionally, the review covers several defense enzymes and proteins in the human body that are important anti-glycating systems acting to prevent the development of neurodegenerative diseases.

3

History of BSE in Poland

86%

Polak M. P., Zmudzinski J. F.

Polish Food

|

2010

|

nr 1

4

Paracrine interactions between non-activated N9 microglial cells in co-culture with SN56 cholinergic neuronal cells

86%

Gul-Hinc S., Ronowska A., Bielarczyk H., Szutowicz A.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

Microglial cells, through the proinflammatory mediators play an important role in host defense and tissue repair in CNS. They contribute to pathomechanisms of Alzheimer’s and other neurodegenerative diseases. The aim of this work was to investigate modifying effects of non-activated migroglia on cholinergic neuronal SN56 cells subjected to common neuroprotective and/or neurotoxic signals. Chronic exposure to Zn or SNP caused loss of viability (30%), inhibition of pyruvate dehydrogenase (PDH) (40%), isocitrate dehydrogenase (60 and 50%) and aconitase activities as well as decrease of acetyl-CoA levels. These alterations in enzyme activities displayed strong direct correlation with depletion of acetylCoA (r=0.86, P<0.0001) and inverse correlation with cell viability (r=0.87, P<0.0001). Resveratrol, free radical scavenger, increased viability of Zn/SNP treated cholinergic cells but did not overcome suppresive effects of SNP and Zn on enzymes activities. Under same neurotoxic conditions, N9 microglial cells cultured on isoporated inserts and added to neuronal culture dishes, also overcame neurotoxic effect Zn and SNP maintaining control levels of acetyl-CoA, enzymes activites and high cell viability. These data sugest that in some specific, pathologic conditions, non-activated microglia may protect neuronal cholinergic neurons against neurotoxic insults by paracrine-like mechanism by protecting their energy metabolism. On the other hand resveratrol neuroprotection may depend on entirely different yet undefined mechanism. Supported by GUMed MN-15, MNiSW NN401029937, IP2010035370, GUMed ST-57 projects.

5

The role of 14-3-3 proteins in neurodegenerative diseases, trafficking and nuclear signalling

86%

Aitken A., Baxter H. C., Forster J., Dubois T.

Cellular and Molecular Biology Letters

|

2000

|

tom 05

|

nr 2

6

Genistein exerts a cell-protective effect via Nrf2/HO-1/ /PI3K signaling in A-beta 25-35-induced Alzheimer’s disease models in vitro

72%

Yi S., Chen S., Xiang J., Tan J., Huang K., Zhang H., Wang Y., Wu H.

Folia Histochemica et Cytobiologica

|

2021

|

tom 59

|

nr 1

7

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Caring for patients with Huntington disease - a survey of caregivers’ experiences and views

72%

Domaradzki J.

Journal of Pre-Clinical and Clinical Research

|

2015

|

tom 09

|

nr 2

Introduction. Despite the growing interest in the consequences of caring for patients with Huntington disease (pHD), little is known about the family caregivers of such patients in Poland. Identification of their needs can improve caregivers’ wellbeing, the quality of care and condition of pHD. The aim of this study was to understand the social functioning of family caregivers of pHD and their perception of the caregiving role. Materials and methods. Data was collected from 55 family caregivers of pHD. A structured questionnaire was used consisting of 86 questions subsumed into five domains: ‘Problems’ and ‘Feelings related to caregiving’, ‘Attitude toward caregiving’, ‘Satisfaction with life’ and ‘Perception of healthcare services’. Correlations between the different scales and other characteristics were measured as potential predictors of the burden. Non-parametric statistical methods were used in the analysis. Results. Most respondents experienced a high (50.9%) or moderate (30.95%) feeling of burden. Although 70.9% of caregivers perceived caregiving positively, for many it was a source of negative feelings. Only 10.9% of respondents declared that caregiving decreased their QoL. Carers’ perception of caregiving was mostly influenced by their negative experiences with the healthcare system. Respondents’ domicile, religious practices, age, income, marital status, time of diagnosis and of caregiving, patient’s age and stage of disease also influenced their experiences. Conclusions. Health professionals and policy planners should focus on monitoring caregivers’ health, identifying their needs, sources of distress, and supporting caregivers’ coping strategies. They should also be better educated about the clinical and practical aspects of HD.

8

Immunoexpression of the selected compounds of the SMN complex in spinal cord neurons in patients with sporadic amyotrophic lateral sclerosis (sALS)

72%

Dziewulska D., Sulejczak D., Chrzanowska H., Ogonowska W., Rafalowska J.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease leading to degeneration and loss of motoneurons in the spinal cord anterior horns. Although etiology of the disease is unknown there is a hypothesis assuming that survival motor neuron protein (SMN) may save motoneurons from degeneration not only in spinal muscular atrophy (SMA) but also in ALS. In animal models of ALS the neuroprotective role of SMN was observed but it is not known whether the phenomenon is present in humans. Therefore we decided to examine immunoexpression of SMN and functionally associated with it gemin 2, 3 and 4 in the anterior horn neurons of patients with sporadic form of ALS (sALS). Material and methods: The material was composed of 10 spinal cords of patients with sALS who died at the age of 52–87 years 1–8 years after the onset of the disease. On formalin-fixed and paraffin-embedded spinal cords immunohistochemistry was applied. The immunohistochemical reactions were performed with antibodies against SMN and gemin 2, 3 and 4 according to the avidin-biotin-peroxidase method. Results: In all the examined cases expression of SMN and gemin 3 in spinal cord neurons was found although intensity of the immune reactions was diverse. The immunolabel were the most intense in patients with acute course of sALS and gradually decreased with longevity of the disease. Not only motoneurons but also interneurons and sensory neurons revealed immunoexpression of SMN and gemin 3. The immune reaction to gemin 2 was negative. The immunoreactivity for gemin 4 was also negative or very weak. Conclusions: (1) In humans, expression of SMN and gemin 3 in neurons is present through the whole lifespan. (2) In sALS, expression of gemin 2 and 4 is abnormal: absent or diminished respectively. (3) Presence of all components of the SMN-gemin complex is probably necessary for its normal functioning. (4) Since the immunoreactivity for SMN, and gemin 2, 3 and 4 was similar in all the examined cases and 6 from the 10 cases were at the age of 65–87 years it seems that advanced age has no influence on expression of the investigated proteins. This study was supported by the Ministry of Science and Higher Education grant NN 401 014640

9

Preclinical development of treatments for tauopathies: translation to the clinic and back

72%

Riedel G.

Acta Neurobiologiae Experimentalis

|

2019

|

tom 79

|

nr Suppl.1

Given the urgent need for a disease modifying treatment of Alzheimer’s disease (AD), there is increasing interest in tau‑based therapeutics. In a comparative study, methylthioninium chloride (MTC) and leucomethylthioninium salts (LMTX®) (5‑75 mg/kg; oral administration for 3-8 weeks) were assessed preclinically in two novel transgenic tau mouse lines (Line 1, Line 66). Behavioural and histopathological proxies were evaluated. Both MTC and LMTX® dose-dependently rescued the learning impairment and restored behavioural flexibility in a spatial problem‑solving water maze task in Line1 and corrected motor‑learning in Line 66. Simultaneously, both drugs reduced the number of tau-reactive neurons, particularly in the hippocampus and entorhinal cortex in Line 1 and had more widespread effects in Line 66. The data establish that diaminophenothiazine compounds like MTC can reverse both spatial and motor learning deficits and reduce the underlying tau pathology and therefore offer potential for the treatment of tauopathies. In the clinic, symptomatic treatments with cholinesterase inhibitors and/or memantine are relatively ineffective and the need for new treatments targeting the underlying pathology of AD is generally recognised. In most of the failed disease-modifying trials conducted over the last 16 years, patients have been allowed to continue taking symptomatic treatments at stable doses, under the assumption that they do not impair efficacy because the modes of action are different. In recently completed Phase 3 trials testing the tau aggregation inhibitor leuco-methylthioninium bis (hydromethanesulfonate) (LMTM), we found highly significant differences in treatment response according to whether patients were taking LMTM as monotherapy (benefit) or as add‑on to symptomatic treatments (no effect). A large body of preclinical research has then been undertaken in wild-type mice and in our tau transgenic mouse model (Line 1) expressing the core tau unit of the AD paired helical filament with the aim of understanding the mechanisms responsible for the reduced efficacy of LMTM as an add‑on to symptomatic treatments. A range of experimental paradigms were used to measure the effects of chronic pretreatment with the cholinesterase inhibitor rivastigmine given for 2-5 weeks prior to adding LMTM treatment for a further 2‑6 weeks. In tau transgenic mice, LMTM given alone was found to increase hippocampal acetylcholine (ACh) levels, glutamate release from synaptosomal preparations, synaptophysin levels in multiple brain regions, mitochondrial complex IV activity, reduce tau pathology, restore choline acetyl transferase (ChAT) immunoreactivity in basal forebrain, and reverse deficits in spatial learning. Chronic pretreatment with rivastigmine was found to reduce or eliminate almost all LMTM treatment effects, apart from reduction in tau aggregation pathology and restoration of ChAT immunoreactivity in the basal forebrain. LMTM effects on hippocampal ACh and levels of synaptophysin were also reversed in wild‑type mice. Collectively, targeting tangles consisting of MAPT protein tau is a viable strategy in preclinical models and was forward translated to AD patients receiving monotherapy. In the clinic, however, prior symptomatic treatment with a cholinesterase inhibitor prohibited the efficacy of LMTM. Back translation to our tau mouse model reproduced this negative interaction and revealed a mechanistic action across different transmitter systems and at multiple compartmental levels of neural function.

10

Effects of IFN-beta1a and IFN-beta1b treatment on the expression of cytokines, inducible NOS (NOS type II), and myelin proteins in animal model of multiple sclerosis

72%

Lubina-Dabrowska N., Stepien A., Sulkowski G., Dabrowska-Bouta B., Langfort J., Chalimoniuk M.

Archivum Immunologiae et Therapiae Experimentalis

|

2017

|

tom 65

|

nr 4

11

Relationships between typical histopathological hallmarks and the ferritin in the hippocampus from patients with Alzheimer’s disease

72%

Kwiatek-Majkusiak J., Dickson D. W., Tacik P., Aoki N., Tomasiuk R., Koziorowski D., Friedman A.

Acta Neurobiologiae Experimentalis

|

2015

|

tom 75

|

nr 4

Oxidative stress is one of the possible mechanisms of neurodegeneration. One of the elements of this mechanism are altered iron homeostasis and changes concerning of iron metabolism regulatory proteins. The primary iron storage protein in cells is ferritin, composed of heavy (H) and light (L) chains. In brain tissue neurons contain mainly ferritin H-chains, whereas glial cells are rich in L-chains. To the best of our knowledge, this is the first study that compares structure of ferritin and histopathological hallmarks in hippocampal tissue affected by the pathological process of Alzheimer’s disease (AD). Our data indicate a statistically significant correlation between the concentration of L chains of ferritin, the H/L ratio and the amount of senile plaques in the subiculum, CA1 and CA4 sectors of the hippocampus (p<0.001, p=0.025, p=0.029). A significant correlation was also found between the concentration of L-ferritin and neuronal loss (p=0.0026). These findings indicate an important role of ferritin light chains in neurodegeneration, that is linked to chronic inflammation processes and the associated activation of the microglia rich of L chains.

12

Inhibitory effect of alpha-lipoic acid on mitochondrial dysfunction and interleukin-8 expression in interleukin-1beta-stimulated ataxia telangiectasia fibroblasts

72%

Yoon J., Lee H., Lim J. W., Kim H.

Journal of Physiology and Pharmacology

|

2020

|

tom 71

|

nr 1

13

Immunoreactivities of some proteins forming SMN protein complex within spinal cord in rat model of fALS

72%

Rafalowska J., Sulejczak D., Gadamski R., Wojda R., Mordzewska-Lewczuk M., Dziewulska D.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

Introduction: Amyotrophic lateral sclerosis (ALS) is a major neurodegenerative disease to afflict the adult human population. ALS causes a progressive motoneuron degeneration within anterior horns of the spinal cord. Recent data indicate the presence of mutations in the SMN (Survival Motor Neuron) gene that cause a deficits in the level of the functional SMN protein and may be an exacerbating factor in the disease development of rat model of fALS. SMN forms the multiprotein complex with selected gemins (i.a. gemin 2, 3 and 4). It is known, that the complex is important for motoneuron development in ontogenesis as well as in the proper functioning of mature motoneuron. However, the level of the SMN and individual gemin expression during the life both in humans and rats still become uncovered. The aim of our study was to determine the immunoreactivities of SMN and gemins 2, 3 and 4 in rat model of fALS during all life span. Material and method: Male rats mutated in SOD-1 were subjected to experiments. Animals at age of 60 days (group 1), 90 days (group 2), 120 days (group 3) were asymptomatic. The last group involving symptomatic rats was created from animals older than 120 days. Rats were perfused in deep anaesthesia. The spinal cords were removed and processed in routine histological staining techniques as well as in immunohistochemical methods (to detect SMN and selected gemins proteins). Labelling sections of spinal cords were analyzed with light and fluorescent microscope. Result: SMN and all investigated gemins were present in spinal cord motoneurons in rats from all experimental groups. However, the level of staining was weaker in the paretic rats. In the opposition to other examined proteins the immunoreaction of gemin 2 was weaker starting from 90 day of life. Conclusion: The SMN protein complex is present in motoneurons within the spinal cord during all animal lifespan in the rat model of familiar ALS. This study was supported by the Ministry of Science and Higher Education grant NN 401 014640

14

Tandemly repeated trinucleotides - comparative analysis

72%

Piwowar M., Meus J., Piwowar P., Wisniowski Z., Stefaniak J., Roterman I.

Acta Biochimica Polonica

|

2006

|

tom 53

|

nr 2

Characteristics of 64 possible tandem trinucleotide repeats (TSSR) from Homo sapiens (hs), Mus musculus (mm) and Rattus norvegicus (rn) genomes are presented. Comparative analysis of TSSR frequency depending on their repetitiveness and similarity of the TSSR length distributions is shown. Comparative analysis of TSSR sequence motifs and association between type of motif and its length (n) using ρ-coefficient method (quantitatively measuring the association between variables in contingency tables) is presented. These analyses were carried out in the context of neurodegenerative diseases based on trinucleotide tandems. The length of these tandems and their relation to other TSSR is estimated. It was found that the higher repetitiveness (n) the lower frequency of trinucleotides tandems. Differences between genomes under consideration, especially in longer than n=9 TSSR were discussed. A significantly higher frequency off A- and T-rich tandems is observed in the human genome (as well as in human mRNA). This observation also applies to mm and rn, although lower abundant in proportion to human genomes was found. The origin of elongation (or shortening) of TSSR seems to be neither frequency nor length dependent. The results of TSSR analysis presented in this work suggest that neurodegenerative disease-related microsatellites do not differ versus the other except the lower frequency versus the other TSSR. CAG occurs with relatively high frequency in human mRNA, although there are other TSSR with higher frequency that do not cause comparable disease disorders. It suggests that the mechanism of TSSR instability is not the only origin of neurodegenerative diseases.

15

How do neurons degenerate in prion diseases or transmissible spongiform encephalopathies [TSEs]: neuronal autophagy revisited

72%

Liberski P. P., Gajdusek D. C., Brown P.

Acta Neurobiologiae Experimentalis

|

2002

|

tom 62

|

nr 3

16

Molecular biology of prions

72%

Weissmann C., Enari M., Klohn P. C., Rossi D., Flechsig E.

Acta Neurobiologiae Experimentalis

|

2002

|

tom 62

|

nr 3

17

Alzheimer's disease and acetylcholine receptors

72%

Kihara T., Shimohama S.

Acta Neurobiologiae Experimentalis

|

2004

|

tom 64

|

nr 1

18

Macrophages and HIV-1-associated dementia

72%

Boven L. A.

Archivum Immunologiae et Therapiae Experimentalis

|

2000

|

tom 48

|

nr 4

19

Analysis of BSE monitoring system in Lithuania

72%

Maciulskis P., Lukauskas K., Sederevicius A., Pridotkas G., Kiudulas V., Pockevicius A., Jonaitis E.

Medycyna Weterynaryjna

|

2008

|

tom 64

|

nr 04A

Lithuania has been strengthening its BSE monitoring program since July 2001. A total of 264,268 cattle were examined during the period of 2001-2006. No BSE positive case was found. A total of 93.1% of healthy slaughtered cattle, 6.3% of fallen stock, 0.4% of emergency slaughtered cattle and 0.2% of cattle with clinical signs were tested at ante mortem inspection. The number of tested adult cattle has increased 4.5 times from 4.17% in 2001 to 18.88% in 2006. 2.41% adult cattle were tested in 2002, 1.97% in 2003, 10.59 % in 2004 and 18.92% in 2005. The number of tested healthy slaughtered adult cattle has increased 4 times from 4.09% in 2001 to 17.41% in 2006. 2.11% of healthy slaughtered adult cattle were tested in 2002, 1.5% in 2003, 9.96% in 2004 and 17.66% in 2005. The number of tested risk group adult cattle has increased 18 times from 0.08% in 2001 to 1.47% in 2006. 0.3% of risk group of adult cattle were tested in 2002, 0.47% in 2003, 0.63% in 2004 and 0.96% in 2005. 94.3% of all tested cattle were from 2 to 11 years old, 0.1% of them were less than 2 years old, 3.0% were 12 years old and 2.6% were 13 years old and more. 54.3% of all tested cattle were more than 5 years old. A total of 53.9% of healthy slaughtered cattle, 59.0% of fallen stock, 61.9% emergency slaughtered cattle and 62.6% of cattle with clinical signs at ante mortem inspection were more than 5 years old. Significant correlation was found between the age of healthy slaughtered cattle and emergency slaughtered cattle and cattle with clinical signs at ante mortem inspection (P < 0.05). There was no correlation between the age of fallen stock and healthy slaughtered cattle. The mean age of healthy slaughtered cattle was 6.5 years and the mean age of fallen stock was 6.7 years in 2005. Enfer TSE and Bio-Rad rapid tests were applied for BSE monitoring. Inconclusive test results were subjected to histopathological and immunocytochemical examination.

20

Medicinal plants affecting the central nervous system - a better understanding of the pharmacological activity

72%

Ozarowski M., Mrozikiewicz P. M.

Herba Polonica

|

2007

|

tom 53

|

nr 2

Ograniczanie wyników

The role of dendritic cells in neurodegenerative diseases

The role of advanced glycation end products in various types of neurodegenerative disease: a therapeutic approach

History of BSE in Poland

Paracrine interactions between non-activated N9 microglial cells in co-culture with SN56 cholinergic neuronal cells

The role of 14-3-3 proteins in neurodegenerative diseases, trafficking and nuclear signalling

Genistein exerts a cell-protective effect via Nrf2/HO-1/ /PI3K signaling in A-beta 25-35-induced Alzheimer’s disease models in vitro

Caring for patients with Huntington disease - a survey of caregivers’ experiences and views