Wyniki wyszukiwania

1

Plasma homocysteine level and the course of ischemic stroke

100%

Pniewski J., Chodakowska-Zebrowska M., Wozniak R., Stepien K., Stafiej A.

Acta Neurobiologiae Experimentalis

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2003

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tom 63

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nr 2

2

Pharmacological caspase inhibitors: research towards therapeutic perspectives

86%

Kudelova J., Fleischmannova J., Adamova E., Matalova E.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 4

3

Exuberant cellular reaction of the optic nerves in experimental Creutzfeldt-Jakob disease

86%

Liberski P. P., Sikorska B., Bratosiewicz-Wasik J., Walis A., Brown P., Brown D.

Acta Neurobiologiae Experimentalis

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2003

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tom 63

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nr 4

4

Genetic aspects of Alzheimer's disease

86%

Zekanowski C., Religa D., Graff C., Filipek S., Kuznicki J.

Acta Neurobiologiae Experimentalis

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2004

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tom 64

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nr 1

5

The role of alpha-synuclein in regulation of cyclin dependent kinase 5

72%

Czapski A. G., Gassowska M., Kazmierczak A., Adamczyk A.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Alpha-Synuclein (ASN), a small cytosolic protein enriched in synaptic terminals, was implicated in the pathomechanism of several neurodegenerative disorders called alpha-synucleinopathies. ASN was shown to be a main component of characteristic intraneuronal protein aggregates called Lewy bodies (LB) and Lewy neurites (LN), observed i.a. in Parkinson’s disease, dementia with LBs and in the LB variant of Alzheimer’s disease. Recent studies demonstrated that ASN may exist also in the extracellular space. Low-molecular ASN aggregates distributed in the brain parenchyma likely may be more toxic than ASN in LB, however, the exact mechanism of cytotoxicity of extracellular ASN is not fully understood. Our previous studies demonstrated the significant impact of extracellular ASN on calcium homeostasis. ASN evoked deregulation of intracellular calcium concentration leading in consequence to enhancement of nitric oxide synthesis. Deregulation of calcium homeostasis affects other calcium-dependent enzymes, including Calpains. The aim of the present study was to investigate the involvement of Calpaindependent activation of Cyclin Dependent Kinase 5 (Cdk5) in molecular mechanism of extracellular ASN cytotoxicity. The activation of Cdk5 is regulated by binding of regulatory subunits p35 and p39. Deregulation of calcium homeostasis may induce the Calpainmediated breakdown of Cdk5/p35 into Cdk5/p25 leading to overactivation of Cdk5. In our studies we used rat Pheochromocytoma PC12 cells incubated with exogenous ASN (10 µM) in the presence of Calpain inhibitor Calpeptin (10 µM) and Cdk5 inhibitors Roscovitine (10 µM) and BML-259 (10 µM). Our results indicated that incubation of PC12 cells in the presence of extracellular ASN (10 µM) for 48 h evoked cell death, and Cdk5 inhibitors efficiently prevented ASN toxicity, indicating an important role of Cdk5 in molecular mechanism of ASN toxicity. The level of Cdk5 protein was unchanged, but phosphorylation of Cdk5 at Tyr15 was significantly increased, suggesting that the enzymatic activity of Cdk5 is increased in ASN-treated cells. The presence of p25 protein was observed, what suggests that Calpain-dependent proteolysis of p35 occurred in ASN-treated cells. Calpeptin, an inhibitor of Calpains, prevented ASN-induced cell death, confirming the important role of Calpain activation in mechanism of ASN toxicity. In summary, our results demonstrated that alteration of calcium homeostasis evoked by extracellular ASN induce Calpain-dependent overactivation of Cdk5. These molecular processes may be involved in ASN-evoked cell death in vitro and probably also in neurodegenerative disorders.

6

Molecular mechanism of PC12 cell death evoked by sodium nitroprusside, a nitric oxide donor

72%

Pytlowany M., Strosznajder J. B., Jesko H., Cakala M., Strosznajder R. P.

Acta Biochimica Polonica

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2008

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tom 55

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nr 2

339-347

Nitric oxide (NO) is a potent extracellular and intracellular physiological messenger. However, NO liberated in excessive amounts can be involved in macromolecular and mitochondrial damage in brain aging and in neurodegenerative disorders. The molecular mechanism of its neurotoxic action is not fully understood. Our previous data indicated involvement of NO in the release of arachidonic acid (AA), a substrate for cyclo- and lipoxygenases (COX and LOX, respectively). In this study we investigated biochemical processes leading to cell death evoked by an NO donor, sodium nitroprusside (SNP). We found that SNP decreased viability of pheochromocytoma (PC12) cells in a concentration- and time-dependent manner. SNP at 0.1 mM caused a significant increase of apoptosis-inducing factor (AIF) protein level in mitochondria. Under these conditions 80% of PC12 cells survived. The enhancement of mitochondrial AIF level might protect most of PC12 cells against death. However, NO released from 0.5 mM SNP induced massive cell death but had no effect on protein level and localization of AIF and cytochrome c. Caspase-3 activity and poly(ADP-ribose) polymerase-1 (PARP-1) protein levels were not changed. However, PARP activity significantly decreased in a time-dependent manner. Inhibition of both COX isoforms and of 12/15-LOX significantly lowered the SNP-evoked cell death. We conclude that AIF, cytochrome cand caspase-3 are not responsible for the NO-mediated cell death evoked by SNP. The data demonstrate that NO liberated in excess decreases PARP-1 activity. Our results indicate that COX(s) and LOX(s) are involved in PC12 cell death evoked by NO released from its donor, SNP.

7

Family-based association analysis of the MAPT gene in Parkinson disease

72%

Wang K. S., Mullersman J. E., Liu X. F.

Journal of Applied Genetics

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2010

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tom 51

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nr 4

The MAPT gene has been shown to be associated with several neurodegenerative disorders, including forms of parkinsonism and Parkinson disease (PD), but the results reveal population differences. We investigated the association of 10 single-nucleotide polymorphisms (SNPs) in the region of MAPT on chromosome 17q21 with PD and age at onset, by using 443 discordant sib pairs in PD from a public dataset (Mayo-Perlegen LEAPS Collaboration). Association with PD was assessed by the FBAT using generalized estimating equations (FBAT-GEE), while the association with age at onset as a quantitative trait was evaluated using the FBAT-logrank statistic. Five SNPs were significantly associated with PD (P < 0.05) in an additive model, and 9 SNPs were associated with PD (P < 0.05) in dominant and recessive models. Interestingly, 8 PD-associated SNPs were also associated with age at onset of PD (P < 0.05) in dominant and recessive models. The SNP most significantly associated with PD and age at onset was rs 17649641 (P = 0.015 and 0.021, respectively). Two-SNP haplotypes inferred from rs 17563965 and rs 17649641 also showed association with PD (P = 0.018) and age at onset (P = 0.026). These results provide further support for the role of MAPT in development of PD.

8

Growth factor gene delivery for Alzheimer's disease: from animal models to clinical trials

72%

Tuszynski M., Nagahara A., Schroeder B., Coppola G., Wang L., Blesch A., Rockenstein E., Geschwind D., Masliah E., Koo E., Chiba A.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

Nervous system growth factors have extensive effects on neuronal function and survival. Nerve growth factor (NGF) prevents the death and stimulates the function of basal forebrain cholinergic neurons in correlational models of Alzheimer’s disease (AD), leading to its translation to Phase 1 and 2 human clinical trials. Separately, Brain-Derived Neurotrophic Factor (BDNF) infl uences the survival and function of entorhinal cortical and hippocampal neurons in several animal models of AD, including transgenic mutant APP-expressing mice; aged rats and lesioned rats; and aged and lesioned primates. These benefi cial effects appear to occur independent of alteration in beta amyloid load. We are currently examining the extended safety and tolerability of BDNF gene delivery to the entorhinal cortex in additional animal studies, potentially leading to specifi c targeting of short term memory loss in future human AD trials. This talk will review the history and current status of growth factor gene delivery in AD and other neurodegenerative disorders.

9

Techniques of human embryonic stem cell and induced pluripotent stem cell derivation

72%

Lewandowski J., Kurpisz M.

Archivum Immunologiae et Therapiae Experimentalis

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2016

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tom 64

|

nr 5

10

The influence of BDNF on human umbilical cord blood stem/progenitor cells: Implications for stem cell-based therapy of neurodegenerative disorders

72%

Paczkowska E., Luczkowska K., Piecyk K., Roginska D., Pius-Sadowska E., Ustianowski P., Cesarska E., Dolegowska B., Celewicz Z., Machalinski B.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr 2

Umbilical cord blood (UCB)-derived stem/progenitor cells (SPCs) have demonstrated the potential to improve neurologic function in different experimental models. SPCs can survive after transplantation in the neural microenvironment and induce neuroprotection, endogenous neurogenesis by secreting a broad repertoire of trophic and immunomodulatory cytokines. In this study, the influence of brain-derived neurotrophic factor (BDNF) pre-treatment was comprehensively evaluated in a UCB-derived lineage-negative (Lin-) SPC population. UCB-derived Lin- cells were evaluated with respect to the expression of i) neuronal markers using immunofluorescence staining and ii) specific (TrkB) receptors for BDNF using flow cytometry. Next, after BDNF pre-treatment, Lin- cells were extensively assessed with respect to apoptosis using Western blotting and proliferation via BrdU incorporation. Furthermore, NT-3 expression levels in Lin- cells using RQ PCR and antioxidative enzyme activities were assessed. We demonstrated neuronal markers as well as TrkB expression in Lin- cells and the activation of the TrkB receptor by BDNF. BDNF pre-treatment diminished apoptosis in Lin- cells and influenced the proliferation of these cells. We observed significant changes in antioxidants as well as in the increased expression of NT-3 in Lin- cells following BDNF exposure. Complex global miRNA and mRNA profiling analyses using microarray technology and GSEA revealed the differential regulation of genes involved in the proliferation, gene expression, biosynthetic processes, translation, and protein targeting. Our results support the hypothesis that pre-treatment of stem/progenitor cells could be beneficial and may be used as an auxiliary strategy for improving the properties of SPCs.

11

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Chromosomal localization of genes encoding small heat shock proteins (HSPB) in cattle and sheep

72%

Danielak-Czech B., Kozubska-Sobocinska A., Babicz M.

Annales Universitatis Mariae Curie-Skłodowska. Sectio EE: Zootechnica

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2015

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tom 33

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nr 4

12

Codon 129 polymorphism of the PRNP gene in normal Polish population and in Creutzfeldt-Jakob disease, and the search for new mutations in PRNP gene

72%

Bratosiewicz J., Liberski P. P., Kulczycki J., Kordek R.

Acta Neurobiologiae Experimentalis

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2001

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tom 61

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nr 3

13

Molecular biology of brain aging and neurodegenerative disorders

72%

Wisniewski T., Frangione B.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

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nr 1

14

Elevated expression of alpha7 neuronal nicotinic acetylcholine receptor during the early stages of damage by oxidative stress in the aging rat brain

58%

Dorszewska J., Rozycka A., Helias-Rodzewicz Z., Kempisty B., Grzelak T., Ziemnicka K., Oczkowska A., Steinborn B., Jagodzinski P.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Aging is accompanied by a high level of oxidized form of guanine, 8-oxo-2’deoxyguanosine (8-oxo-2’dG), and decreased level of 8-oxoguanine glycosylase 1 (OGG1) in the brain. The development and progression of neurodegenerative disorders are also characterized by dysfunction or loss of the brain nicotinic acetylcholine receptors (nAChRs). To study whether the differences in nAChRs expression in the rat brain occur due to aging or oxidative stress we analyzed RNA and protein levels of α7, α4 and β2 subunits by RQ-PCR and Western blot validation in three brain structures: cerebral grey matter (CGM), sub-cortical white matter (SCWM) and cerebellum (Ce) of twenty one female Wistar rats. The first group consisted of five 3.0–3.5-month-old females, which was assigned as a young control group. The remaining sixteen females aged of 18–24 month were divided into three following groups: (1) aged control group of 5 rats; (2) a vehicle group of 5 rats which received intraperitoneal injections of deionized water; (3) memantine-treated group of 6 rats. In each group, the selected brain areas have also been analyzed to determinate the levels of oxidative stress. In this study, age- and stress- dependent differential RNA and protein expression levels were approved only in OGG1 and α7 nAChR proteins. In all analyzed brain structures of young and old controls, the levels of oxidized form of guanine were similar. Stress relevant to water injection increased the level of 8-oxo-2’dG in the cerebellum of old control rats (Ce, P<0.05). The old controls demonstrated an important reduction of OGG1 mRNA expression in CGM and Ce regions compared to young individuals (CGM P=0.03; Ce P=0.2). Western blot analysis has also revealed a reduction of OGG1 protein in the sub-cortical white matter of old individuals (SCWM, P=0.03). However, there was no important influence of water administration on OGG1 expression in all brain regions. In all analyzed brain structures, expression of α7 nAChR was down-regulated in old controls compared to young controls. However, this decrease was only significant in SCWM area (SCWM, P<0.05). Treatment with H2O caused a significant increase in RNA and protein levels of α7 nAChR in SCWM as compared to this brain structure of the aged control rats (SCWM, P<0.01). Our results suggest that aging of the rat brain is mostly associated with decreased expression of OGG1 as well as with deficit of α7 nAChR in the sub-cortical white matter. Stress relevant to water injection increases the level of 8-oxo-2’dG in the aging rat brain, but clearly overcomes the α7 nAChR deficit. A significant increase of the α7 nAChR expression in the SCWM of H2O-treated rats suggests that these receptors play an important role in compensatory mechanisms facilitating the impaired cholinergic neurotransmission following oxidative stress in the aging rat brain.

15

Neuroprotective effects of dehydroepiandrosterone (DHEA) in rat model of Alzheimer's disease

58%

Aly H. F., Metwally F. M., Ahmed H. H.

Acta Biochimica Polonica

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2011

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tom 58

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nr 4

The current study was undertaken to elucidate a possible neuroprotective role of dehydroepiandrosterone (DHEA) against the development of Alzheimer's disease in experimental rat model. Alzheimer's disease was produced in young female ovariectomized rats by intraperitoneal administration of AlCl3 (4.2 mg/kg body weight) daily for 12 weeks. Half of these animals also received orally DHEA (250 mg/kg body weight, three times weekly) for 18 weeks. Control groups of animals received either DHAE alone, or no DHEA, or were not ovariectomized. After such treatment the animals were analyzed for oxidative stress biomarkers such as hydrogen peroxide, nitric oxide and malondialdehyde, total antioxidant capacity, reduced glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase and catalase activities, antiapoptotic marker Bcl-2 and brain derived neurotrophic factor. Also brain cholinergic markers (acetylcholinesterase and acetylcholine) were determined. The results revealed significant increase in oxidative stress parameters associated with significant decrease in the antioxidant enzyme activities in Al-intoxicated ovariectomized rats. Significant depletion in brain Bcl-2 and brain-derived neurotrophic factor levels were also detected. Moreover, significant elevations in brain acetylcholinesterase activity accompanied with significant reduction in acetylcholine level were recorded. Significant amelioration in all investigated parameters was detected as a result of treatment of Al-intoxicated ovariectomized rats with DHEA. These results were confirmed by histological examination of brain sections. These results clearly indicate a neuroprotective effect of DHEA against Alzheimer's disease.

16

Mechanobiology of the brain in health and disease

58%

Sheridan G. K.

Acta Neurobiologiae Experimentalis

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2019

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tom 79

|

nr Suppl.1

Basic research into neurodegenerative disorders, like Alzheimer’s disease, is heavily focused on understanding genetic susceptibility and biochemical triggers of pathology, as well as disturbances to the intrinsic electrophysiological properties of affected neurons. Often overlooked is the role of mechanics, particularly mechanical properties and mechano‑sensitivity/‑responsiveness of neurons and glia. Recent evidence confirms that mechanical signals regulate CNS development and pathophysiology. In this talk, I will discuss the role of mechanics in both physiological and pathophysiological brain ageing. A defining pathophysiological hallmark of Alzheimer’s disease is the amyloid plaque; an extracellular deposit of aggregated fibrillar Aβ1‑42 peptides. Amyloid plaques are hard, brittle structures scattered throughout the hippocampus and cerebral cortex and are thought to cause hyperphosphorylation of tau, neurofibrillary tangles, and progressive neurodegeneration. Glia are highly mechanosensitive cells and can sense the mismatch between the normally soft mechanical environment of the brain and very stiff amyloid plaques via mechanosensing ion channels. Both ageing and peripheral infection augment amyloid plaque‑induced upregulation of mechanoresponsive ion channels in astrocytes. Further research is required to investigate whether modulating mechanically-gated channel opening will protect or exacerbate the disease state, and most importantly, if they are novel drug targets for age‑related dementia

17

The role of sphingosine kinases/sphingosine-1-phosphate in the regulation of alpha-synuclein and amyloid beta precursor protein secretion. Implications for neurodegenerative disorders

58%

Jesko H., Okada T., Nakamura S., Strosznajder R. P.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

|

nr 1

Sphingolipid deregulation may be an important factor of age-related neuronal stress vulnerability. Current data suggests potential links between sphingosine kinases (SphK1&2), their product sphingosine1-phosphate (S1P) and age-related protein conformation diseases. The aim of this study was to investigate a possible role of SphKs in alpha-synuclein (ASN) and amyloid beta (ABeta) precursor protein (APP) level and secretion. The studies were carried out using human SH-SY5Y neuroblastoma cell line stably transfected with the human gene for α-synuclein (ASNwt). Sphingosine kinase inhibitor (SKI) significantly increased ASN secretion in concentration-dependent manner. S1P also displayed similar influence. Neither compound exerted any significant effect on the ASN protein level. S1P may act via cell surface receptors or as an intracellular second messenger. The similar effect of S1P and SphK inhibitors on ASN secretion may suggest that the regulation of its release is critically dependent on the varied (intra)cellular targets of SphKs and downstream signaling pathways. We have found that stable human ASNwt expression in SH-SY5Y cells caused a three-fold, significant increase of the cellular APP level. In ASN-transfected cells S1P enhanced APP secretion and reduced its intracellular level. This could be linked to the recently reported effect of S1P on secretase beta activity. Inhibition of SphKs significantly decreased APP secretion. In summary our data indicates that endogenous ASN regulates APP level in SH-SY5Y cells and that sphingolipids play a crucial role in the secretion of ASN and APP. These processes may have significant impact on neuronal survival and health.

18

In search for effective modulators of the proteasome activity

58%

Karpowicz P., Stoj J., Gaczynska M., Osmulski P., Jankowska E.

Acta Neurobiologiae Experimentalis

|

2013

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tom 73

|

nr 1

Proteasome is a multi-activity enzyme involved in a ubiquitin-dependent turnover of cytoplasmic and nuclear proteins. It recognizes and digests short-lived regulatory proteins, influencing cellular processes as crucial as progression of the cell cycle, transcription, oncogenesis and flux of substrates through metabolic pathways. The enzyme is responsible also for the housekeeping chores, degrading misfolded or oxidatively damaged proteins. Defects in the proteasome action play a causal role in development of a number of diseases, among which are cerebral ischemia and neurodegenerative disorders such as Huntington’s, Alzheimer’s, and Parkinson’s diseases. Being a multifunctional proteolytic machinery, the proteasome must act under a strict control to prevent massive degradation of all intracellular proteins, which would result in a cell death. One of the levels of such a control is the proteasome structure itself. The core particle called 20S proteasome is a barrel-like structure made up of four rings of seven subunits each. The outer (α) rings play predominantly a structural role forming a kind of a gated channel leading to the proteolytic chamber. The inner-β-rings harbor six active sites, concealed inside the cavity formed by the β subunits. So far, the only proteasome-targeting agents used in clinics are competitive inhibitors, directly blocking the enzyme’s active sites. However, the multi-subunit barrel-like structure of the 20S proteasome encourages to test compounds which can target allosteric interactions between subunits and influence the gating mechanism, involved in the control of the substrates’ uptake. Such modulators may provide a precise and substrate-specific regulation of the proteasome catalytic performance. Additionally, targeting the allosteric interactions may enable not only inhibition but also stimulation of the proteasome, which is crucial in managing disorders connected with the proteasome not sufficient activity, such as neurodegenerative diseases. A variety of protein ligands, interacting with the outer ring of the 20S proteasome and modulating its activity, is already known. They can serve as templates for design of putative small-molecule allosteric drugs. In an effort to find synthetic compounds able to enhance or suppress the performance of the proteasome active centers we utilize one of such protein ligands – HIV-1 Tat protein. The protein is known to inhibit the core proteasome and to interfere with the physiological PA28 activator in its binding to the 20S. G48RKKRRQRRRPS59 fragment of HIV-1 Tat (Tat1) occurred to be very efficient in the 20S proteasome inhibition. By single and multiple alanine substitutions we have recognized “hot spots” in the sequence of Tat1. NMR and molecular dynamics calculations allowed us to correlate these putative pharmacophores with the structural turns. By introduction of a non-peptide turn-inducing modification to the Tat1 sequence we have obtained the derivatives highly toxic for human cultured cancer cells HeLa.S3. The work was supported by grants: NCN 2011/01/B/ST5/06616 and DS/8440-4-0172-2

19

Extracellular alpha-synuclein contributes to gsk-3beta-dependent Tau phosphorylation in PC12 dopaminergic cells: Its role in pathomechanism of Parkinson’s disease

58%

Gassowska M., Czapski G. A., Adamczyk A.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

|

nr 1

alpha-Synuclein (ASN) play important role in pathogenesis of Parkinson’s disease (PD) and other neurodegenerative disorders. Novel and most interesting data showed elevated tauopathy in PD and suggested relationship between ASN and Tau protein. However, the mechanism of ASN-evoked Tau protein modification is not fully elucidated. In this study, we investigated the role of glycogen synthase kinase-3β (Gsk-3β) and cyclin-dependent kinase 5 (Cdk5) in ASN-evoked Tau modification in dopaminergic PC12 cells. We used real-time quantitative PCR (qRT-PCR) analysis to assess Gsk3β gene expression and Western blot technique to analyse protein phosphorylation. The presence of apoptotic cells was assessed by Hoechst 33258 fluorescent staining, and cell viability was determined by the 2-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay. Our data showed that exogenously added ASN (10 μM) increases Tau phosphorylation on Ser396 and specific Gsk-3β inhibitor (SB-216763, 10 µM) opposite to Cdk5 inhibitor protects cells against Tau hyperphosphorylation. Western blot analysis showed that ASN affected Gsk-3β via increasing of protein level and activation of this enzyme. From immunochemical studies, was found that ASN treatment leads to significant increase in GSK-3β immunoreactivity by about 20%. GSK-3β activity evaluated by its phosphorylation status assay showed that ASN significantly increased the phosphorylation of this enzyme at Tyr216 with parallel decrease in phosphorylation at Ser9, indicative of stimulation of GSK-3β activity. ASN-induced apoptotic processes leads to decrease of PC12 cells viability, the apoptotic cells determined by phase contrast together with Hoechst 33258 fluorescent staining, indicated significantly increase of apoptosis in the presence of ASN. SB-216763 prevented ASN-induced cytotoxicity and enhanced PC12 cell viability. In conclusion, all these findings suggested that extracellular ASN is involved in Gsk-3β-dependent Tau modulation and its proapoptotic effect might be mediated at least in part by the Gsk-3β catalysed Tau hyperphosphorylation and impairment of cytoskeleton stability. GSK-3β inhibitors may offer promising tool against ASN-induced Tau modification and cytotoxicity in neurodegenerative disorders. Supported by statutory theme 9.

20

Docosahexaenoic acid provides protective mechanism in bilaterally MPTP-lesioned rat model of Parkinson's disease

58%

Hacioglu G., Seval-Celik Y., Tanriover G., Ozsoy O., Saka-Topcuoglu E., Balkan S., Agar A.

Folia Histochemica et Cytobiologica

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2012

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tom 50

|

nr 2

Ograniczanie wyników

Plasma homocysteine level and the course of ischemic stroke

Pharmacological caspase inhibitors: research towards therapeutic perspectives

Exuberant cellular reaction of the optic nerves in experimental Creutzfeldt-Jakob disease

Genetic aspects of Alzheimer's disease

The role of alpha-synuclein in regulation of cyclin dependent kinase 5

Molecular mechanism of PC12 cell death evoked by sodium nitroprusside, a nitric oxide donor

Family-based association analysis of the MAPT gene in Parkinson disease

Growth factor gene delivery for Alzheimer's disease: from animal models to clinical trials

Techniques of human embryonic stem cell and induced pluripotent stem cell derivation

The influence of BDNF on human umbilical cord blood stem/progenitor cells: Implications for stem cell-based therapy of neurodegenerative disorders

Chromosomal localization of genes encoding small heat shock proteins (HSPB) in cattle and sheep

Codon 129 polymorphism of the PRNP gene in normal Polish population and in Creutzfeldt-Jakob disease, and the search for new mutations in PRNP gene

Molecular biology of brain aging and neurodegenerative disorders

Elevated expression of alpha7 neuronal nicotinic acetylcholine receptor during the early stages of damage by oxidative stress in the aging rat brain

Neuroprotective effects of dehydroepiandrosterone (DHEA) in rat model of Alzheimer's disease

Mechanobiology of the brain in health and disease

The role of sphingosine kinases/sphingosine-1-phosphate in the regulation of alpha-synuclein and amyloid beta precursor protein secretion. Implications for neurodegenerative disorders

In search for effective modulators of the proteasome activity

Extracellular alpha-synuclein contributes to gsk-3beta-dependent Tau phosphorylation in PC12 dopaminergic cells: Its role in pathomechanism of Parkinson’s disease

Docosahexaenoic acid provides protective mechanism in bilaterally MPTP-lesioned rat model of Parkinson's disease