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T. vaginalis a występowanie grzybów i dwoinki rzeżączki w populacji łódzkiej. VII Ogólnopolskie Sympozjum Przeciwrzęsistkowe, Łódź, 27-28 VI 1980

100%
Slaska M., Wieckowska A.
Wiadomości Parazytologiczne
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1981
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tom 27
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nr 2
2

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

81%
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.
3

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

71%
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.
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Diet-derived changes in insulin metabolism in brain accelerate the development of Alzheimer's disease neuropathological features

71%
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
|
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.
5

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

61%
Wieckowska A., Mietelska-Porowska A., Wydrych M., Dlugosz J., Chutoranski D., Wojda U.
Acta Neurobiologiae Experimentalis
|
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.
6

Sardynia kraina angloarabow

50%
Figari C., Wieckowska A.
Koń Polski
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1993
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tom 28
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nr 2
12
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