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Research paper

MULTINOMIAL LOGISTIC REGRESSION APPROACH FOR THE EVALUATION OF BINARY DIAGNOSTIC TEST IN MEDICAL RESEARCH

Alok Kumar Dwivedi, Indika Mallawaarachchi, Juan B. Figueroa-Casas, Angel M. Morales, Patrick Tarwater

Statistics in Transition New Series, Volume 16 , ISSUE 2, 203–222

review-article | 30-November-2020

Effects of vitamin E on neurodegenerative diseases: an update

mechanisms behind neurodegeneration, even though the causes of AD, PD, ALS and stroke have not been fully explained (Behl, 1999; Abou-Sleiman et al., 2006). In addition, it is believed that oxidative stress may increase the risk of progression of neurodegenerative diseases by causing abnormal protein folding and function (Bossy-Wetzel et al., 2004; Ricciarelli et al., 2007). Ischemia triggers processes that increase free radical formation through different pathways. Firstly, glutamate, which activates

Mehmet Arif Icer, Neslihan Arslan, Makbule Gezmen-Karadag

Acta Neurobiologiae Experimentalis, Volume 81 , ISSUE 1, 21–33

Review | 06-February-2018

Nigrostriatal interaction in the aging brain: new therapeutic target for Parkinson’s disease

striatum. Newly discovered striatal neurogenesis – normally a lifelong process – determines the efficiency of nigrostriatal interaction. Deficient neurogenesis within the striatum followed by a decline in the GABAergic/dopaminergic interaction results in progressive disconnection of the dopaminergic input, which initiates a ‘vicious circle’ cascade of neuronal damage. Effects of both deficient striatal neurogenesis and age-related neurodegeneration within the striatum accumulate, resulting in a

Janusz W. Błaszczyk

Acta Neurobiologiae Experimentalis, Volume 77 , ISSUE 1, 106–112

research-article | 26-March-2021

Aminoguanidine ameliorates ovariectomy-induced neuronal deficits in rats by inhibiting AGE-mediated Aβ production

well-known AGE inhibitor, is a nucleophilic hydrazine compound that prevents AGE formation. AG has been reported to inhibit inflammatory reactions and reduce potential neurodegeneration in numerous experimental dementia models (Rodrigues et al., 2009). It has also been suggested that AG prevents cognitive impairment and reduces glial activation in the brain of mice with dementia induced by streptozotocin. Additionally, the beneficial effects of AG on the CNS include the suppression of AGE receptors

Dan Di Zhang, Yan Gang Wang, Chun Yan Liu, Ze Hou Wang, Yue Fen Wang

Acta Neurobiologiae Experimentalis, Volume 81 , ISSUE 1, 10–20

Review | 31-July-2017

The physiology of blood platelets and changes of their biological activities in multiple sclerosis

Barbara Wachowicz, Agnieszka Morel, Elżbieta Miller, Joanna Saluk

Acta Neurobiologiae Experimentalis, Volume 76 , ISSUE 4, 269–281

research-paper | 14-June-2019

Selective neuronal death following exposure to methylenedioxypyrovalerone is accompanied by an inhibition of NMDA receptor NR2B subunit expression

implicated in reward and addiction, the neurodegeneration elicited by the drug is likely related to its emotional and rewarding effects. One of the candidate targets are N-methyl-D-aspartate receptors (NMDAR) which are known to undergo developmental alteration (maturation) and also display functional plasticity. We, therefore, investigated the alterations of NMDAR subunit distribution by measuring the expression levels of receptor proteins in the NAc of 7-day-old mice, 24 hours after systemic bolus

László István Gerecsei, Tamás Balázsa, Diego Echevarría, Ágota Ádám, Gergely Zachar, András Csillag

Acta Neurobiologiae Experimentalis, Volume 79 , ISSUE 1, 92–100

research-article | 30-November-2018

The interplay between parkin and alpha-synuclein; possible implications for the pathogenesis of Parkinson’s disease

express significant levels of α-syn (Jęśko et al., 2017). Transport of α-syn to neighboring cells has been reported to propagate neurodegeneration (Desplats et al., 2009). α-syn is sometimes likened to the prion protein due to its ability to transfer between different types of cells, and refold from the physiological α-helix-rich conformation into an oligomerization-prone β-sheet structure, (Jęśko et al., 2017). The role of parkin in secretion of α-syn into the extracellular space has not been studied

Henryk Jęśko, Anna M. Lenkiewicz, Anna Wilkaniec, Agata Adamczyk

Acta Neurobiologiae Experimentalis, Volume 79 , ISSUE 3, 277–290

research-article | 30-November-2019

A smaller olfactory bulb in a mouse model of Down syndrome

Pietro Bontempi, Barbara Cisterna, Manuela Malatesta, Elena Nicolato, Carla Mucignat-Caretta, Carlo Zancanaro

Acta Neurobiologiae Experimentalis, Volume 80 , ISSUE 4, 375–380

research-article | 15-October-2020

Serum levels of hepcidin and interleukin 6 in Parkinson’s disease

INTRODUCTION The pathology of Parkinson’s disease (PD) is considered to be multifactorial. In addition to causing alterations in protein transformation, genetic defects and mitochondrial disfunction, the disease also induces chronic neuroinflammation and elevated oxidative stress processes. Neurodegeneration in PD is associated with complex relationships between immune-inflammatory pathways and peripheral tissues. Evidence for peripheral and central chronic inflammation in patients with PD

Jolanta Kwiatek-Majkusiak, Maciej Geremek, Dariusz Koziorowski, Ryszard Tomasiuk, Stanisław Szlufik, Andrzej Friedman

Acta Neurobiologiae Experimentalis, Volume 80 , ISSUE 3, 297–304

research-article | 30-November-2019

Roux-en-Y gastric bypass surgery triggers rapid DNA fragmentation in vagal afferent neurons in rats

establish the order of neurodegenerative responses in vagal afferents after RYGB in the NG and NTS in male and female rats. We tested the hypothesis that RYGB surgery induces neurodegeneration initially in the periphery (vagal perikarya located in the NG) rather than more central locations, i.e. NTS. We further hypothesized that RYGB triggers rapid withdrawal of vagal afferents and increases microglia activation in the NTS. Because previous studies have shown that markers of injury and neuronal death

Dulce M. Minaya, Patricia M. Di Lorenzo, Andras Hajnal, Krzysztof Czaja

Acta Neurobiologiae Experimentalis, Volume 79 , ISSUE 4, 432–444

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