Review
A number of studies have demonstrated that rural living and exposure to pesticides such as dichlorodiphenyltrichloroethane (DDT) highly increase the chances of developing Parkinson’s disease. In a previous work, we have found that DDT leads to the formation of vesicular buds that are released from the cells upon fusion of an intermediate endocytic compartment with the plasma membrane. Since extracellular vesicles like exosomes have been implicated in the development of neurodegenerative
Mario Rossi,
Marco Scarselli,
Irene Fasciani,
Roberto Maggio,
Franco Giorgi
Acta Neurobiologiae Experimentalis , ISSUE 2, 113–117
research-article
Introduction:
Parkinson’s disease (PD) is a progressive neurological disorder caused by the loss of dopamine producing cells in the substantia nigra, which is located in the basal ganglia. As dopamine assists with transmitting and modulating signals in the brain, ongoing dopamine depletion causes motor, autonomic and cognitive impairments (Magrinelli et al., 2016). PD is characterised by motor symptoms that are associated with movement (e.g. bradykinesia, rigidity, postural instability, tremor
Vincent Carroll,
Kirsten Deutschmann,
Jessica Andrews
Australasian Journal of Neuroscience , ISSUE 1, 32–43
Review
Parkinson’s disease (PD) is a progressive neurodegenerative disorder of unclear etiology and pathogenesis. Research results gathered to date support the hypothesis that the motor symptoms of the disease result from the gradual loss of midbrain dopamine neurons residing in the substantia nigra pars compacta (SNpc). Recent discoveries, however, significantly expand this knowledge indicating that the primary source of the PD pathogenesis may be located both in the SNpc as well as in the GABAergic
Janusz W. Błaszczyk
Acta Neurobiologiae Experimentalis , ISSUE 1, 106–112
Article
Introduction
Definition
“Lewy body dementia” (LBD) is broadly considered to consist of two related disorders-Parkinson’s disease dementia (PDD) and dementia with Lewy bodies (DLB) (Connors et al., 2017). Neuro-pathologically, these spectrum disorders are characterised by the widespread distribution of aggregated a-synuclein, forming structures called Lewy bodies in neuronal cell bodies and processes (Galasko, 2017; Stubendorrf, Aarsland, Minthon & Londos, 2012). The abnormal clumping and
Madelaine B Rañola
Australasian Journal of Neuroscience , ISSUE 1, 5–12
research-article
INTRODUCTION
Parkinson’s disease (PD) is one of the most common age-related neurodegenerative disorders. Despite years of intense research and testing of candidate treatments, all available therapies are symptomatic. The long period of stealthy, relatively symptom-free development is shared with other neurodegenerative disorders (notably, with Alzheimer’s disease – AD), and hampers diagnosis, elucidation of disease mechanisms, and possible therapy (reviewed in Jęśko et al., 2017). The main
Henryk Jęśko,
Anna M. Lenkiewicz,
Anna Wilkaniec,
Agata Adamczyk
Acta Neurobiologiae Experimentalis , ISSUE 3, 277–290
case-report
Background:
An 80 year old man with advanced Parkinson’s disease (PD) was admitted to the neuroscience unit with a worsening decline in mobility. Medical management was the commencement and titration of the levodopacarbidopa intestinal gel (LCIG) Duodopa ® via a naso-jejunal tube, which had been inserted under fluoroscopy in Interventional Radiology. Over a ten day trial period the patient responded well to the administration of the LCIG with much less periods of difficulty with movement (known
Rachael Elizabeth Mackinnon
Australasian Journal of Neuroscience , ISSUE 2, 1–4
Research paper
Mutations in the PINK1 gene are responsible for typical symptoms of Parkinson’s disease. Using Drosophila melanogaster mutant PINK1B9 and after PINK1 silencing with RNAi using transgenic lines, we observed defects in synapses and behavior. The lack or reduced expression of PINK1 prolonged sleep during the day (nap) and decreased the total locomotor activity during 24 h, in addition to a decrease in climbing ability and a reduced lifespan. In the brain, PINK1 mutants had a lower level of
Bartosz Doktór,
Milena Damulewicz,
Wojciech Krzeptowski,
Barbara Bednarczyk,
Elżbieta Pyza
Acta Neurobiologiae Experimentalis , ISSUE 3, 231–241
Research paper
Parkinson’s disease (PD) is a common neurodegenerative disorder, resulting from progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNc). Neuroprotective therapies in PD are still not available, perhaps because animal models do not imitate the chronic and progressive nature of the clinical state of PD. To address this, we performed a feasibility study aimed at establishing a chronic non-primate large animal PD model in Göttingen minipigs based on continuous infusion
Mette Slot Nielsen,
Andreas Nørgaard Glud,
Arne Møller,
Poul Mogensen,
Dirk Bender,
Jens Christian Sørensen,
Doris Doudet,
Carsten Reidies Bjarkam
Acta Neurobiologiae Experimentalis , ISSUE 3, 199–211
case-report
unaffected father and a carrier mother.
While the underlying mechanisms of DBS are not yet fully understood, it allows changes in brain activity to be made in a controlled manner (Herrington, Cheng & Eskandar 2016). Prior to DBS surgical lesioning was the primary surgical intervention for Parkinson’s Disease (PD) and dystonic conditions. This involves the insertion of a heated electrode into structures within the basal ganglia, destroying cells within a very small area and disrupting electrical brain
Vincent Cheah
Australasian Journal of Neuroscience , ISSUE 1, 7–10
Research paper
The subthalamic nucleus (STN) is important for normal movement as well as in movement disorders. The STN is a target nuclei in patients with advanced Parkinson’s disease (PD). Deep brain stimulation (DBS) is a standard surgical treatment for PD. Although DBS results in a significant reduction in motor disability, several negative side effects have been reported. Thus, to understand the side effects of DBS the connection of the STN should be well known. Therefore, the present study aims to re
Safiye Çavdar,
Merve Özgür,
Yusuf Özgür Çakmak,
Yasemin Kuvvet,
Sıla Kezban Kunt,
Gökay Sağlam
Acta Neurobiologiae Experimentalis , ISSUE 3, 251–263