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1

Alzheimer's disease as a calciumopathy

100%

Wojda U.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr S

Alzheimer’s disease (AD) is the most common age-related neurodegenerative dementia attributed to the amyloid beta (Aβ) deposition in the brain. Analysis of rare familiar (FAD) cases with mutations in presenilin, the proteins responsible for generation of Aβ from its precursor APP, firmed the ‘amyloid hypothesis’ of AD etiology. However, anti-amyloid therapies failed indicating that AD pathogenesis is more complex and involves additional mechanisms. Affected brain areas of AD patients and of animal FAD models showed increased levels of intracellular Ca2+, alterations in expression levels of Ca2+- signaling proteins and increased activation of Ca2+-dependent enzymes. Based on these data, the ‘Ca2+ hypothesis of AD’ has been proposed. Ca2+ contributes to the development of AD by Ca2+-triggered ER and mitochondrial dysfunction, and Ca2+- dependent changes in gene expression. The elevated cytosolic Ca2+ levels affect synaptic stability and function, and can activate death signaling. Moreover, the augmented cellular Ca2+ levels affect Aβ generation. In turn, Aβ generation potentiate Ca2+ dyshomeostasis in several ways. For example, Aβ causes impairment of NMDARs signaling while the released APP intracellular domain modulates Ca2+ homeostasis as the regulator of IP3-mediated Ca2+ efflux from the ER. Mutant presenilins contribute to Ca2+ dyshomeostasis as impaired ER Ca2+ leak channels and via interactions with Ca2+-signaling proteins such as calsenilin. Taken together, a growing body of evidence indicates that AD pathogenesis is based on the interplay between Ca2+ dyshomeostasis and neuropathological hallmarks of AD such as Aβ and mutated PS1. Thus, stabilizers of neuronal Ca2+ homeostasis and signaling may have therapeutic potential for AD treatment.

2

Circulating micrornas in blood as biomarkers of early Alzheimer’s disease

100%

Wojda U.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

Among the major challenges related to Alzheimer’s disease (AD) is identifying biomarkers of the early AD stage in easily accessible blood samples, as an alternative to existing sophisticated (brain imaging) and invasive (cerebrospinal fluid, CSF) procedures for AD diagnosis. One of the promising approaches concentrates on circulating microRNAs (miRNAs). Using qRT-PCR we compared the miRNA profiles in the blood plasma of 15 mild cognitive impairment patients with early AD (MCI-AD), whose diagnoses were confirmed by CSF biomarkers, with 20 later AD patients and 15 non-demented, age-matched individuals (CTR). In the first screening, we assessed 179 plasma miRNAs. We confirmed 23 miRNAs reported earlier as AD biomarker candidates and found 26 novel differential miRNAs. For 15 statistically significant differential miRNAs, the TargetScan, MirTarBase and KEGG database analysis indicated putative targets among key proteins involved in AD pathology such as MAPT (tau), APP and enzymes of amyloidogenic proteolysis. These 15 miRNAs were verified in separate, subsequent AD, MCI-AD and CTR groups. Finally, 6 miRNAs were selected as the most promising biomarker candidates differentiating early AD from controls with the highest fold changes (from 1.32 to 14.72), consistent significance, specificities from 0.78 to 1 and sensitivities from 0.75 to 1), (patent pending, PCT/IB2016/052440). The identified miRNA panel in the blood could not only serve as an early non-invasive AD diagnostic, but could also indicate individualized therapy. FINANCIAL SUPPORT: This research was supported by the EU Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement no 665735 (Bio4Med) and by the funding from the Polish Ministry of Science and Higher Education (agreement no 3548/ H2020/COFUND/2016/2). The work was carried out with the use of CePT infrastructure financed by the European Regional Development Fund within the Operational Programme “Innovative economy” for 2007–2013.

3

Terapia genowa komorek ukladu krwiotworczego: rozwoj strategii i wektorow

100%

Wojda U.

Postępy Biologii Komórki

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2004

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tom 31

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nr 2

245-257

4

Aneuploidy, chromosomal missegregation, and cell cycle reentry in Alzheimer's disease

63%

Zekanowski C., Wojda U.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 2

232-253

Alzheimer's disease (AD) is a neurodegenerative disorder with a complex etiology and pathogenesis. Chromosome missegregation was proposed two decades ago to be responsible for neurodegeneration in AD patients. It was speculated that the aneuploidy is a result of aberrant cell cycle of neuronal progenitors during adult neurogenesis and/or of mature neurons. There is mounting evidence of increased rate of general aneuploidy and cell cycle reentry in the AD patients' brains, with area-specific pattern. In this review, we discuss the involvement of chromosome instability, genome damage and cell cycle impairment in AD pathology.

5

Biochemical properties of calcyclin - a potential marker of some diseases

63%

Wojda U., Kuznicki J.

Acta Biochimica Polonica

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1993

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tom 40

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nr 1

6

Kalcyklina - Bialko wiazace wapn z rodziny S-100

51%

Filipek A., Wojda U., Lesniak W., Kuznicki J.

Postępy Biochemii

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1996

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tom 42

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nr 2

213-217

7

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Choroba Alzheimera jako efekt niezdrowej diety: rola insulinooporoności mózgu

51%

Domanska J., Mietelska-Porowska A., Wojda U.

Wszechświat

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2023

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tom 124

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nr 01-03

8

Influence of systemic inflammation and fluctuations of blood glucose level on amyloidopathy progression in mouse model of sporadic Alzheimer’s disease

51%

Wieckowska A., Wydrych M., Mietelska-Porowska A., Wojda U.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

INTRODUCTION: Prominent neuropathologic features of Alzheimer’s Disease (AD) are the appearance of senile plaques composed of amyloid peptides and neurofibrillary tangles derived from Tau protein. Induction of main risk factors before the appearance of typical neuropathological AD hallmarks can help to track the sequence of different and complicated early molecular mechanisms of the sporadic form of human AD (SAD). AIM(S): Our aim is to establish a mouse model that would mimic molecular mechanisms leading to SAD by induction of systemic neuroinflammation and insulin resistance in transgenic mice with mutated human gene encoding amyloid precursor protein (Tg APP). Additionally, we would like to check whether the same experimental conditions may induce AD hallmarks in wild type mice, that may be a proof of lifestyle factors influence on AD development. METHOD(S): In order to induce neuroinflammation and evaluate the influence of insulin dysregulation in the brain, Tg APP and C57BL mice were injected with LPS, and diabetes was induced by high-fat diet feeding, or streptozocin injection. Every two weeks blood glucose level and body weight were checked. To characterize the metabolic phenotype and immunostaining pattern of neuroinflammatory markers and amyloid β, mice blood and brain tissue were used. RESULTS: We show effects of systemic administration of infectious agent in neuroinflammation in the brain and body weight and blood biochemical pattern related to high-fat diet and their relation with amyloidopathy progression in the brain. CONCLUSIONS: The data verify if lifestyle conditions including ongoing systemic inflammation and metabolic changes related to unhealthy diet may accelerate amyloidopathy progression. Studied factors may cause changes not only in Tg APP mice but also lead to the development of AD hallmarks in brain of mice without mutations in APP gene. Results might provide the evidence that the proposed animal model may be an effective tool to study the molecular mechanisms of early stages of SAD progression. FINANCIAL SUPPORT: Polish National Science Centre Grant 2014/15/D/NZ4/04361.

9

Lipopolysaccharide accelerates neuroinflammation in a mouse model of Alzheimer's disease

45%

Dlugosz J., Wieckowska A., Koperski M., Mietelska-Porowska A., Wojda U.

Acta Neurobiologiae Experimentalis

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2019

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tom 79

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nr Suppl.1

INTRODUCTION: The amyloid hypothesis postulates that the main cause of Alzheimer’s disease (AD) is amyloidogenic cleavage of amyloid precursor protein (APP) and deposition of amyloid‑beta. Recently, another hypothesis was formulated that neuroinflammation may precede amyloid generation in AD development. It was also demonstrated that systemic inflammation may impair brain homeostasis and function. AIM(S): Based on these data we hypothesized that systemic inflammation impairs brain homeostasis and leads to neuroinflammation that later causes AD development. METHOD(S): To verify this hypothesis, we compared effects of systemic inflammation induced by intraperitoneal injection of lipopolysaccharide (LPS) in transgenic mice expressing human APP with Swedish AD-causing mutation (APPswe) to untreated APPswe mice. To assess AD neuropathological hallmarks, brain tissue from 4, 8, and 12‑month old animals were analyzed by immunohistochemical staining and immunoblotting. RESULTS: We found that LPS shortly after peripheral administration to APPswe mice induced astrogliosis and dysregulation of pro- and anti-inflammatory cytokines in brains already in young 4‑month old animals and these effects were also detected in 8-month old mice. In control mice not treated with APPswe, the development of signs of neuroinflammation was slower. We also compared the signs of neuroinflammation in the hippocampus and entorhinal cortex to levels of APP full-length protein and its pathologically truncated CTFs forms. CONCLUSIONS: Obtained results indicate that systemic inflammation accelerates and intensifies neuroinflammation as reflected by astrogliosis and pro-inflammatory reaction during AD development. It suggests that systemic inflammation can be considered as a common civilization risk factor of AD progression. These data became the reference for the next hypothesis and studies of our group (abstracts by A. Mietelska‑Porowska and by A. Więckowska). FINANCIAL SUPPORT: Financed by National Science Center grants no. 2014/15/D/NZ4/04361, 2018/29/N/ NZ7/01724.

10

Brain expression and subcellular localization of Calmyrin 2, a novel Ca-binding protein

45%

Blazejczyk M., Sobczak A., Jaworski J., Kuznicki J., Wojda U.

Acta Neurobiologiae Experimentalis

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2007

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tom 67

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nr 3

11

Diet-derived changes in insulin metabolism in brain accelerate the development of Alzheimer's disease neuropathological features

45%

Mietelska-Porowska A., Wieckowska A., Dlugosz J., Koperski M., Wojda U.

Acta Neurobiologiae Experimentalis

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2019

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tom 79

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nr Suppl.1

INTRODUCTION: The western diet (WD), enriched in saturated fatty acids, cholesterol, and simple carbohydrates., is known to cause metabolic syndrome related to insulin metabolism impairment. On the other hand, metabolic syndrome is described as a potential risk factor for Alzheimer’s disease (AD). Main early AD features in brain are altered proteolysis of amyloid precursor protein (APP) and hyperphosphorylation of tau protein. AIM(S): Our aim was to verify our hypothesis that the WD causes insulin metabolism disturbances and may accelerate development of early AD hallmarks. METHOD(S): To verify this hypothesis, we compared effects of WD feeding (from 3rd month of age) in transgenic mice expressing human APP with Swedish AD-causing mutation (APPswe) compared to APPswe mice in which systemic inflammation was induced by injection of lipopolysaccharide (LPS; the model described in the abstract by J. Dlugosz), and to untreated APPswe mice. To assess AD neuropathological hallmarks, all groups were analysed at the ages of 4, 8, and 12‑months by immunohistochemical and immunoblotting analysis. RESULTS: Our results demonstrate levels of insulin resistance marker and insulin/Aβ degrading enzyme in relation to characteristic neuropathological AD hallmarks, such as occurrence, intensity of staining, and neuronal compartmentalisation of phosphorylated isoform of Tau protein, and the level of APP full-length protein and its pathologically truncated CTFs forms, in the hippocampus and cortex of mice brains. CONCLUSIONS: Obtained results indicate that WD is linked to insulin metabolism impairment and leads to accelerated over-phosphorylation of tau protein and proteolysis of APP. This suggests that the WD, via impairment in insulin metabolism, may accelerate the development of AD. FINANCIAL SUPPORT: Financed by National Science Center grant no. 2014/15/D/NZ4/04361.

12

Porównanie wybranych metod serologicznych do określania poziomu przeciwciał anty-Toxoplasma gondii

45%

Vogtt E., Dzierzanowska D., Wojda U., Jarocka K., Czaplak B.

Diagnostyka Laboratoryjna

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1988

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tom 24

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nr 3

13

Increased vulnerability to oxidative stress in lymphocytes from SAD and FAD patients

45%

Bialopiotrowicz, Kuzniewska B., Kuchamakova N., Kuznicki J., Wojda U.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

Alzheimer’s disease (AD) is the most common neurodegenerative disorder in which certain molecular changes are observed not only in neurons but also in peripheral cells. Growing evidence suggests that AD post-mitotic neurons exhibit increased apoptotic response to oxidative stress, mitochondria dysfunction and calcium dyshomeostasis. We hypothesized that some of these alterations could be observed in peripheral lymphocytes and studied for potential diagnostic purposes. We analyzed apoptotic response to the redox stress evoked by 2-deoxy-Dribose in immortalized lymphocytes from 18 patients with sporadic AD (SAD), from 2 familial AD (FAD) patients with novel mutations in presenilin 1: P117R and I213F, and from 20 agematched healthy individuals. Using two independent fl ow cytometry methods for quantifi cation of apoptosis, we found that SAD and FAD lymphocytes show enhanced apoptotic response to the redox stress. This apoptotic response was accompanied by decline in mitochondrial membrane potential measured with JC-1 as well as by increased activities of caspase 9 and caspase 3. However, no changes in the expression of two calcium-binding proteins: calmyrin 1 and calreticulin were observed. This study emphasizes that increased susceptibility to redox stress and associated upregulation of mitochondrial apoptotic pathway is characteristic not only for AD neurons, but also for AD lymphocytes. Thus, human lymphocytes could be used in further studies on AD pathogenesis.

14

Ca2plus-binding calmyrin is a monomeric protein highly expressed in motoneurons of rat spinał cord

39%

Blazejczyk M., Sobczak A., Piszczek G., Kreutz M. R., Kuznicki J., Wojda U.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 3

15

Western diet - from metabolic disturbances to acceleration of glia activation and development of Alzheimer’s disease

39%

Wieckowska A., Mietelska-Porowska A., Wydrych M., Dlugosz J., Chutoranski D., Wojda U.

Acta Neurobiologiae Experimentalis

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2019

|

tom 79

|

nr Suppl.1

INTRODUCTION: A diet enriched in fat, cholesterol, and sugar – called the Western diet (WD) – was shown to induce systemic inflammation, obesity, and metabolic syndrome and results directly and indirectly in an impact on brain structure and function. The WD has not been examined yet in the context of Alzheimer’s disease (AD), characterised by altered cleavage of amyloid precursor protein (APP) and deposits of toxic amyloid. AIM(S): We aimed to verify the hypothesis that WD by inducing metabolic syndrome and systemic inflammation may accelerate brain glia activation events and the onset of AD. METHOD(S): To verify this hypothesis, transgenic mice expressing human APP with Swedish AD-causing mutation (APPswe) were fed with WD from 3rd month of age. These mice were compared to APPswe mice in which systemic inflammation was induced by injection of lipopolysaccharide (LPS) and to untreated APPswe mice. All animal groups were subsequently analysed at the age of 4, 8, and 12‑months by immunohistochemical and immunoblotting analysis. RESULTS: Already one month of WD feeding induces metabolic disturbances including hypercholesterolemia and hyperglycaemia and accelerates the brain pathological events in young APPswe mice. After one month of WD feeding, we observed enhanced astrogliosis, altered profile of microglia activation state, and enhanced cleavage of APP in mice brains. Moreover, we observed obesity, enhanced liver weight, and non-alcoholic fatty liver disease (NAFLD) after 3 months of the WD, which suggest that the WD causes alterations in the brain even earlier than in peripheral organs. CONCLUSIONS: These results suggest that the WD leads to brain neuroinflammation and accelerates the development of AD. Therefore, the WD can be considered as a newly identified common civilian AD risk factor. FINANCIAL SUPPORT: Supported by National Science Center grants: 2014/15/D/NZ4/04361, 2018/29/N/ NZ7/01724.

16

Structural and biochemical properties of Calmyrin 2, a novel calcium binding protein in the brain

39%

Sobczak A., Blazejczyk M., Debowska K., Cymerman I., Kirilenko A., Pikula S., Wojda U.

Acta Neurobiologiae Experimentalis

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2007

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tom 67

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nr 3

17

Expression regulation of a novel Ca2+ binding protein Calmyrin 2 (Cih2) indicates its function in NMDA receptor mediated Ca2+signaling

39%

Debowska K., Blazejczyk M., Sobczak A., Jaworski J., Kuzmicki J., Wojda U.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

Calmyrin 2 (CaMy2, Cib2) represents a novel calmyrin subfamily of Ca2+ binding proteins that coordinate Ca2+ in the EF-hand motives. CaMy2 mRNA was recently detected in brain, but nothing is known about CaMy2 protein localization and properties in the brain. We have cloned CaMy2 from rat brain, demonstrated CaMy2 Ca2+- sensor properties and determined its neuronal pattern of rat brain expression. CaMy2 protein is expressed mainly in hippocampal neurons and localizes together with Golgi apparatus and dendrite markers. Our studies in primary cultures of hippocampal neurons demonstrate that expression of CaMy2 protein is induced upon neuronal activation with pharmacological agents that stimulate Ca2+ infl ux through such types of Ca2+ channels as glutamate excitatory receptors and voltage-operated Ca2+ channels. In addition, increase in CaMy2 protein level was induced by soluble amyloid β and BDNF. However, most prominent increase in CaMy2 protein (7-fold), and mRNA (2-fold) occurs upon stimulation of NMDA receptor (NMDAR). The induction is blocked by translation inhibitors, specifi c antagonists of NMDAR, the Ca2+-chelator BAPTA, and inhibitors of ERK1/2 and PKC, kinases transmitting NMDAR-linked Ca2+ signal. Our results show that CaMy2 level is controlled by NMDAR and Ca2+ and suggest CaMy2 role in Ca2+ signaling underlying NMDAR activation. This work was supported by the Polish Ministerial Research grant N301 109 32/3854.

18

Cell cycle malfunctions in lymphocytes from sporadic Alzheimer’s disease patients

39%

Bialopiotrowicz E., Kuzniewska B., Kochamakova-Trojanowska N. M., Barcikowska M., Kuznicki J., Wojda U.

Acta Neurobiologiae Experimentalis

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2011

|

tom 71

|

nr 1

Alzheimer’s disease (AD) constitutes one of the leading causes of disability with enormous socioeconomic costs. Most of AD cases occur sporadically and have unknown etiology (SAD). The Abeta peptide deposition in neuritic plaques is one of AD major hallmarks. Nevertheless, the role of Abeta as a primary driver in AD progression arouses controversy. Mounting evidence suggests that neurodegeneration results from the cell cycle reentry occurring in AD neurons. Recent data indicate that some of the cell cycle changes can be also observed in peripheral cells. Thus, our aim was to investigate whether any cell cycle abnormalities occur in transcriptome or proteome of lymphocytes from SAD patients. This study was performed in immortalized lymphocytes from 18 SAD patients and 26 healthy age-matched individuals. PCR arrays experiments showed that 43% of the 90 investigated cell cycle genes were down-regulated in SAD, whereas 4% were up-regulated comparing to control lymphocytes. Since most significant changes referred to the genes engaged in G1/S control, we assessed the levels of key proteins involved in G1/S transition with immunobloting. The most striking difference occurred in p21 protein level, which was significantly elevated for SAD in respect to controls. Furthermore, we measured distribution of cells in G1, S and G2/M cell cycle phases using flow cytometry. Our results showed increased % of cells in G1 phase with adequate decrease in % of cells in S phase for SAD lymphocytes. However, estimation of proliferation rate for SAD and control lymphocytes revealed no significant differences. We therefore used the following methods to assess the lengths of G1 and S phases: flow cytometry analysis of PI-labeled cells after nocodazole treatment and BrdU pulse chase labeling. SAD lymphocytes indicated significant prolongation of G1 phase and simultaneous shortening of S phase. In addition, treating the cells with gamma-secretase inhibitor L685,458 did not affect the observed cell cycle dysregulations, which highlighted that the impairments of cell cycle in SAD lymphocytes are not linked to gamma-secretase activity. Taken together, this study emphasizes that disturbances in the cell cycle control are common for AD neurons as well as SAD lymphocytes. Thus, human lymphocytes could be used in further studies on AD pathogenesis and diagnostics

19

Beyond amyloid:altered cell cycle regulation in Alzheimer's disease:comparison of P21 signaling in patients lymphocytes and brain neurons

39%

Mietelska-Porowska A., Wojsiat J., Laskowska-Kaszub K., Stepien T., Wierzba-Bobrowicz T., Wojda U.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

|

nr Supl.

BACKGROUND AND AIMS: Alzheimer’s disease (AD) develops for decades, but the molecular mechanism of pathogenesis is poorly understood. In result, an effective AD cure is still missing. According to the cell cycle (CC) hypothesis, one of the AD causes is CC reactivation in mature neurons. We aimed at elucidation if similar CC alterations occur in AD brain neurons and in peripheral blood cells. METHODS: As the study materials, we used 40 lines of immortalized lymphoblasts from sporadic AD (SAD) patients and 40 lines from healthy non-demented individuals (controls)1-4. CC in lymphocytes was analyzed by real-time PCR-arrays, immunoblotting, and flow cytometry. Human post mortem brain tissue from AD patients was prepared by paraffin embedding and microscopic tissue slides of hippocampus and enthorinal cortex was analyzed by antip21 immunohistochemical staining. RESULTS: Our data demonstrated aberrant CC in SAD lymphoblasts that involved a prolongation of the G1 phase driven by a marked increase of levels of p21 protein (Walf1/Cip1/Sid1), the key regulator of the G1/S CC checkpoint and of apoptosis. Consistently, we also found differences in p21 levels and its signaling pathway in apoptotic response of SAD lymphoblasts to redox stess. The analysis of p21 protein levels and related signaling in AD brain neurons will also be presented. CONCLUSIONS: In summary, these studies indicate that p21-related molecular changes underlie altered cell cycle and apoptosis in AD pathology and may represent novel therapeutic targets. Moreover, our data show that AD have a features of a systemic disease with CC alterations in peripheral lymphoblasts which thus have a potential diagnostic value. Support: CEPT, Polish National Science Centre grant NN401 596840, and JPND grant 2/BIOMARKAPD/JPND/2012.

20

Alterations in apoptotic signaling in lymphocytes of patients in early stage of Alzheimer's disease precede massive neuronal loss in the brain

39%

Wojsiat J., Laskowska-Kaszub K., Mandecka M., Gabryelewicz T., Kuznicki J., Wojda U.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

|

nr Supl.

BACKGROUND AND AIMS: Alzheimer’s disease (AD) is the most common age-related dementia worldwide of unclear early pathogenesis. Mild Cognitive Impairment (MCI) represents an early AD stage, preceding massive deposition of Aβ aggregates and associated neuronal loss in the brain. Recently we demonstrated that sporadic AD (SAD) lymphoblasts show increased levels of p21 protein, the key regulator of G1/S cell cycle checkpoint and apoptosis (Bialopiotrowicz et al. 2011, Neurobiol Aging). In the current study we aimed to elucidate if p21 levels are altered early in AD, in lymphocytes of MCI patients, and to investigate the effects of p21 on the apoptotic response of SAD and MCI lymphocytes METHODS: We compared apoptotic response to 2 deoxy-D ribose (2dRib) in EBV-immortalized B-lymphoblasts from 16 patients with SAD, 17 patients with MCI and 10 age-matched healthy individuals without dementia. Apoptotic response was measured using flow cytometry assays: AnnexinV, mitochondrial membrane potential, and SubG1-phase. RESULTS: Comparing to controls, under basal conditions p21 levels assessed by immunoblotting were significantly elevated in MCI lymphoblasts, similarly as in SAD cells. 24 h after 2dRib treatment, apoptosis was higher in SAD cells than in controls, and after stimulation p21 decreased significantly in SAD and MCI cells. CONCLUSIONS: SAD lymphoblasts are significantly lessresistant to oxidative apoptotic stimuli than controls. In MCI lymphoblasts there were similar tendencies but without statistical significance. These results suggest that changes in the p21 levels and in apoptotic response in lymphocytes appear early in AD and gradually increase with the disease progression. Furthermore, our data indicate that lymphocytes may be useful for the development of new early AD diagnostic markers based on apoptotic regulatory proteins such as p21. This research was supported by the grant 2/BIOMARKAPD/ JPND/2012 and by the Nencki Institute statutory funds.

Ograniczanie wyników

Alzheimer's disease as a calciumopathy

Circulating micrornas in blood as biomarkers of early Alzheimer’s disease

Terapia genowa komorek ukladu krwiotworczego: rozwoj strategii i wektorow

Aneuploidy, chromosomal missegregation, and cell cycle reentry in Alzheimer's disease

Biochemical properties of calcyclin - a potential marker of some diseases

Kalcyklina - Bialko wiazace wapn z rodziny S-100

Choroba Alzheimera jako efekt niezdrowej diety: rola insulinooporoności mózgu

Influence of systemic inflammation and fluctuations of blood glucose level on amyloidopathy progression in mouse model of sporadic Alzheimer’s disease

Lipopolysaccharide accelerates neuroinflammation in a mouse model of Alzheimer's disease

Brain expression and subcellular localization of Calmyrin 2, a novel Ca-binding protein

Diet-derived changes in insulin metabolism in brain accelerate the development of Alzheimer's disease neuropathological features

Porównanie wybranych metod serologicznych do określania poziomu przeciwciał anty-Toxoplasma gondii

Increased vulnerability to oxidative stress in lymphocytes from SAD and FAD patients

Ca2plus-binding calmyrin is a monomeric protein highly expressed in motoneurons of rat spinał cord

Western diet - from metabolic disturbances to acceleration of glia activation and development of Alzheimer’s disease

Structural and biochemical properties of Calmyrin 2, a novel calcium binding protein in the brain

Expression regulation of a novel Ca2+ binding protein Calmyrin 2 (Cih2) indicates its function in NMDA receptor mediated Ca2+signaling

Cell cycle malfunctions in lymphocytes from sporadic Alzheimer’s disease patients

Beyond amyloid:altered cell cycle regulation in Alzheimer's disease:comparison of P21 signaling in patients lymphocytes and brain neurons

Alterations in apoptotic signaling in lymphocytes of patients in early stage of Alzheimer's disease precede massive neuronal loss in the brain