Wyniki wyszukiwania

1

Cystatin C and neuropeptid Y levels in brain tissues after experimental subarachnoid hemorrhage

100%

Acikgoz S., Can M., Guven B., Edebali N., Barut F., Buyukuysal C., Tekin I. O., Acikgoz B.

Acta Biochimica Polonica

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2014

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tom 61

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nr 4

2

The role of metabotropic glutamate receptors in Alzheimer's disease

100%

Lee H., Zhu X., O'Neill M. J., Webber K., Casadesus G., Marlatt M., Raina A. K., Perry G., Smith M. A.

Acta Neurobiologiae Experimentalis

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2004

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tom 64

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nr 1

3

NG2 expressing cells in hippocampal cultures survive neurotoxic insult and retain the ability to divide

100%

Dzwonek K.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 2

4

Alzheimer's disease and the cell cycle

100%

Raina A. K., Zhu X., Smith M. A.

Acta Neurobiologiae Experimentalis

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2004

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tom 64

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nr 1

5

Tamoxifen and vitamin E treatments delay symptoms in the mouse model of Niemann-Pick C

100%

Bascunan-Castillo E. C., Erickson R. P., Howison C. M., Hunter R. J., Heidenreich R. H., Hicks C., Trouard T. P., Gillies R. J.

Journal of Applied Genetics

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2004

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tom 45

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nr 4

6

Brain energy metabolism in neurodegeneration of dopaminergic neurons in animal model of early Parkinson's disease: role of astrocytes

84%

Kuter K., Olech L., Glowacka U., Paleczna M., Kosmowska B., Jurga A.

Acta Neurobiologiae Experimentalis

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2019

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tom 79

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nr Suppl.1

Glial pathology and energy metabolism changes in the brain precede symptoms of Parkinson’s disease (PD) and multiple other neurodegenerative diseases. Astrocytes govern and regulate a large part of the energy metabolism in the brain. Prolonged impairment of astrocytic functions could increase the vulnerability of dopaminergic neurons in the substantia nigra (SN). In this model, 40‑50% of dopaminergic neurons were selectively killed, causing transient locomotor disability compensated with time. We also induced death of astrocytes in the SN, simultaneously activating microglia but sparing the dopaminergic neurons. The astrocytes replenished after toxin withdrawal. We studied multiple markers of energy metabolism and mitochondrial oxidative phosphorylation (OxPhos) complex and supercomplex functioning during the early stages of neurodegeneration and compensation in the SN and striatum (STR). Death of astrocytes diminished the capability of the dopaminergic system to compensate for the degeneration of neurons. It caused a local energy deprivation, a shift in the usage of energy substrates, via increased glycogenolysis and glycolysis markers, ketone bodies availability, and fatty acid transport in remaining glial cells. Increased neuronal expression of CPT1c and astrocytic expression of CPT1a suggest adaptation in fatty acid use. On the other hand, lesion of dopaminergic neurons influenced OxPhos system and enhanced its functioning. Microglia activation also plays an important role in the processes of degeneration, compensation, and energy metabolism regulation. Modulation of its activation phenotypes might be beneficial towards the indicated processes. Astrocyte and microglia energetic influence is one of the factors in the neuronal compensatory mechanisms of dopaminergic system and might have a leading role in presymptomatic PD stages.

7

Neuropathic alterations of the myenteric plexus neurons following subacute intraperitoneal administration of salsolinol

84%

Kurnik M., Gil K., Gajda M., Thor P., Bugajski A.

Folia Histochemica et Cytobiologica

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2015

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tom 53

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nr 1

8

Ultrastructural features of the neurovascular unit in Alzheimer's neurodegeneration

84%

Frontczak-Baniewicz M., Walski M.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 4

91-96

Recent studies suggest that capillaries, neurons, and astrocytes form a functional unit that serves to maintain cerebral homeostasis. Physiological interactions between all these components of the neurovascular unit control cerebral microcirculation, while abnormal regulatory mechanisms lead to cerebral dysfunction and disease states, such as Alzheimer’s disease (AD). Using electron microscopy, we studied a fragment of the frontotemporal cortex obtained intraoperatively from a patient with established AD. The objective of our study was to assess the ultrastructure of the components of the neurovascular unit. Such ultrastructural studies allow analyzing the structural process of new blood vessels formation and also the appearance of neurons and astrocytes contributing to the neurovascular unit. We suggest that dysfunction of particular components of the neurovascular unit underlies AD and ultimately leads to neurodegeneration.

9

Postconditioning effectively prevents trimethyltin induced neuronal damage in the rat brain

84%

Lalkovicova M., Burda J., Nemethova M., Burda R., Danielisova V.

Folia Biologica

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2016

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tom 64

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nr 2

10

Circadian rhythms of melatonin and cortisol in manifest Huntington's disease and in acute cortical ischemic stroke

84%

Adamczak-Ratajczak A., Kupsz J., Owecki M., Zielonka D., Sowinska A., Checinska-Maciejewska Z., Krauss H., Michalak S., Gibas-Dorna M.

Journal of Physiology and Pharmacology

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2017

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tom 68

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nr 4

11

Acrylamide toxicity and cholinergic nervous system

84%

Kopanska M., Muchacka R., Czech J., Batoryna M., Formicki G.

Journal of Physiology and Pharmacology

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2018

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tom 69

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nr 6

12

Genetic study of familial cases of Alzheimer's disease

84%

Kowalska A., Pruchnik-Wolinska D., Florczak J., Modestowicz R., Szczech J., Kozubski W., Rossa G., Wender M.

Acta Biochimica Polonica

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2004

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tom 51

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nr 1

A small number (1-5%) of Alzheimer's disease (AD) cases associated with the early-onset form of the disease (EOAD) appears to be transmitted as a pure genetic, autosomal dominant trait. To date, three genes responsible for familial EOAD have been identified in the human genome: amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2). Mutations in these genes account for a significant fraction (18 to 50%) of familial cases of early onset AD. The mutations affect APP processing causing increased production of the toxic Aβ42 peptide. According to the "amyloid cascade hypothesis", aggregation of the Aβ42 peptide in brain is a primary event in AD pathogenesis. In our study of twenty AD patients with a positive family history of dementia, 15% (3 of 20) of the cases could be explained by coding sequence mutations in the PS1 gene. Although a frequency of PS1 mutations is less than 2% in the whole population of AD patients, their detection has a significant diagnostic value for both genetic counseling and treatment in families with AD.

13

Melatonin as an antioxidant: biochemical mechanisms and pathophysiological implications in humans

84%

Reiter R. J., Tan D., Mayo J. C., Sainz R. M., Leon J., Czarnocki Z.

Acta Biochimica Polonica

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2003

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tom 50

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nr 4

This brief resume enumerates the multiple actions of melatonin as an antioxidant. This indoleamine is produced in the vertebrate pineal gland, the retina and possibly some other organs. Additionally, however, it is found in invertebrates, bacteria, unicellular organisms as well as in plants, all of which do not have a pineal gland. Melatonin's functions as an antioxidant include: a), direct free radical scavenging, b), stimulation of antioxidative enzymes, c), increasing the efficiency of mitochondrial oxidative phosphorylation and reducing electron leakage (thereby lowering free radical generation), and 3), augmenting the efficiency of other antioxidants. There may be other functions of melatonin, yet undiscovered, which enhance its ability to protect against molecular damage by oxygen and nitrogen-based toxic reac- tants. Numerous in vitro and in vivo studies have documented the ability of both physiological and pharmacological concentrations to melatonin to protect against free radical destruction. Furthermore, clinical tests utilizing melatonin have proven highly successful; because of the positive outcomes of these studies, melatonin's use in disease states and processes where free radical damage is involved should be increased.

14

Alzheimer's amyloid-beta [Abeta] is an essential synaptic protein, not neurotoxic junk

84%

Koudinov A. R., Berezov T. T.

Acta Neurobiologiae Experimentalis

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2004

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tom 64

|

nr 1

15

Gene therapy: panacea or placebo? II. Main applications of gene therapy

84%

Gorecki D. C., MacDermont K. D.

Archivum Immunologiae et Therapiae Experimentalis

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1997

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tom 45

|

nr 5-6

16

The classification of microglial activation phenotypes on neurodegeneration and regeneration in Alzheimer’s disease brain

67%

Varnum M. M., Ikezu T.

Archivum Immunologiae et Therapiae Experimentalis

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2012

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tom 60

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nr 4

17

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Role of iron in pathogenesis of Parkinson disease

67%

Galazka-Friedman J., Friedman A.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2011

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tom 92

|

nr 2

18

Ceramide and sphingomyelin levels are increased in brains of rats exposed to streptozotocin

67%

Prokopiuk S., Fiedorowicz A., Bienias K., Sadowska A., Niemirowicz K., Zendzian-Piotrowska M., Car H.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Insulin insufficiency and increased glucose levels are the major features of diabetes type 1 leading to cognitive dysfunctions and neurodegeneration. A reason why different brain structures are characterized by diverse response to increased glucose level is not known. Our previous study showed increased ceramide levels in the brains of rats with diabetes induced by streptozotocin (STZ) injection, which was abolished by myriocin, the inhibitor of serine palmitylotransferase. Ceramides may be important mediators of neuropathological changes and its elevation was found in many brain disorders. The main goal of our present study was to verify if hippocampus, prefrontal cortex and cerebellum response differently to hyperglycemia/hypoinsulinemia in terms of changes in sphingolipids concentrations. We attempted to identify potential source of ceramides by measuring the sphingomyelinase concentrations and by blocking the ceramide de novo synthesis pathway. We found that in cerebellum and hippocampus of hyperglycemic animals sphingolipids concentrations underwent subtle modifications while prefrontal cortex exhibited massive changes in ceramides and SMs content. Total ceramide levels was significantly elevated in prefrontal cortex of diabetic rats, which was reduced by myriocin, while rats exposed to STZ showed only small increase of total SM in this brain structure. The increased content of ceramides containing SAFAs (saturated fatty acids) in prefrontal cortex was diminished by myriocin. SAFA-contained SMs did not present changes. Elevation of MUFA- (monounsaturated fatty acids), and PUFA-ceramides (polyunsaturated fatty acids) in prefrontal cortex of STZ-treated rats was reduced by myriocin, similarly as MUFA-SMs augmentation. PUFA-ceramides and PUFA-SMs experienced only slight modifications. Both – ceramides and omega-6 – SMs increased dramatically and were downregulated by myriocin. We conclude that the prefrontal cortex may be particularly sensitive to hyperglycemic conditions and hypoinsulinemia. Moreover, the novo synthesis seems to be an important pathway of ceramide generation since usage of myriocin strongly reduced ceramide levels enhanced by STZ injection. Augmentation in ceramide content was correlated with enhancement of SMs production. These unexpected results may be explained by the incorporation of redundant ceramides into SMs, a mechanism by which the toxic level of ceramides is reduced in the brain. Supported by grant 123-27575 P from the State Committee for Scientific Research, Warsaw, Poland

19

Differences in glutathione S-transferase pi expression in transgenic mice with symptoms of neurodegeneration

67%

Kazmierczak B., Kuzma-Kozakiewicz M., Usarek E., Baranczyk-Kuzma A.

Acta Biochimica Polonica

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2011

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tom 58

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nr 4

Glutathione S-transferase pi (GST pi) is an enzyme involved in cell protection against toxic electrophiles and products of oxidative stress. GST pi expression was studied in transgenic mice hybrids (B6-C3H) with symptoms of neurodegeneration harboring SOD1G93A (SOD1/+), Dync1h1 (Cra1/+) and double (Cra1/SOD1) mutations, at presymptomatic and symptomatic stages (age 70, 140, 365 days) using RT-PCR and Western blotting. The main changes in GST pi expression were observed in mice with the SODG93A mutation. In SOD1/+ and Cra1/SOD1 transgenics, with the exception of cerebellum, the changes in GST pi-mRNA accompanied those in GST pi protein. In brain cortex of both groups the expression was unchanged at the presymptomatic (age 70 days) but was lower at the symptomatic stage (age 140 days) and at both stages in hippocampus and spinal cord of SOD1/+ but not of Cra1/SOD1 mice compared to age-matched wild-type controls. In cerebellum of the presymptomatic and the symptomatic SOD1/+ mice and presymptomatic Cra1/SOD1 mice, the GST pi-mRNA was drastically elevated but the protein level remained unchanged. In Cra1/+ transgenics there were no changes in GST pi expression in any CNS region both on the mRNA and on the protein level. It can be concluded that the SOD1G93A but not the Dync1h1 mutation significantly decreases detoxification efficiency of GST pi in CNS, however the Dync1h1 mutation reduces the effects caused by the SOD1G93A mutation. Despite similarities in neurological symptoms, the differences in GST pi expression between SOD1/+ and Cra1/+ transgenics indicate a distinct pathogenic entity of these two conditions.

20

Dynein c1h1, dynactin and syntaphilin expression in brain areas related to neurodegenerative diseases following exposure to rotenone

67%

Chaves R. S., Melo T. Q., D'Unhao A. M., Farizatto K. L. G., Ferrari M. F. R.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 4

Neurodegeneration is often accompanied by protein inclusions which may interfere with cell physiology. On the other hand, alteration in intracellular trafficking may precede impairment of neurotransmission and therefore trigger cell death. In view of this, it is hypothesized that changes in mitochondrial traffic may occur before neurodegeneration triggered by rotenone exposure and could favor this process. The effects of low concentrations of rotenone on the expression of dynein clhl, dynactin and syntaphilin, which are proteins related to mitochondria transport and anchoring, were evaluated in cell cultures of substantia nigra, locus coeruleus and hippocampus as well as in these same brain areas in Lewis aged rats. The results indicate that low concentrations of rotenone decrease dynein clhl protein levels in cell cultures and brain areas of aged rats. Dynactin is decreased after exposure to 0.1 and 0.3 nM of rotenone, and increased after exposure to 0.5 nM of rotenone in cell cultures. Aged rats present increased dynactin expression. Syntaphilin expression decreased in vitro and increased in vivo after rotenone exposure. These findings suggest that changes in protein expression related to mitochondrial retrograde transport and anchoring occur before neurodegeneration induced by rotenone exposure, which may be a primary factor to trigger neurodegenerative mechanisms.

Ograniczanie wyników

Cystatin C and neuropeptid Y levels in brain tissues after experimental subarachnoid hemorrhage

The role of metabotropic glutamate receptors in Alzheimer's disease

NG2 expressing cells in hippocampal cultures survive neurotoxic insult and retain the ability to divide

Alzheimer's disease and the cell cycle

Tamoxifen and vitamin E treatments delay symptoms in the mouse model of Niemann-Pick C

Brain energy metabolism in neurodegeneration of dopaminergic neurons in animal model of early Parkinson's disease: role of astrocytes

Neuropathic alterations of the myenteric plexus neurons following subacute intraperitoneal administration of salsolinol

Ultrastructural features of the neurovascular unit in Alzheimer's neurodegeneration

Postconditioning effectively prevents trimethyltin induced neuronal damage in the rat brain

Circadian rhythms of melatonin and cortisol in manifest Huntington's disease and in acute cortical ischemic stroke

Acrylamide toxicity and cholinergic nervous system

Genetic study of familial cases of Alzheimer's disease

Melatonin as an antioxidant: biochemical mechanisms and pathophysiological implications in humans

Alzheimer's amyloid-beta [Abeta] is an essential synaptic protein, not neurotoxic junk

Gene therapy: panacea or placebo? II. Main applications of gene therapy