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Abstrak :
ABSTRAK
Certaines r gions du cerveau adulte, comme l rsquo;hippocampe, produisent des nouveaux neurones qui participent certaines capacit s d rsquo;apprentissage et de m moire. Dans les maladies neurod g n ratives comme la maladie d rsquo;Alzheimer MA , ils sont alt r s. Dans des souris mod les de la MA, nous avons montr que ces nouveaux neurones souffraient de plus d rsquo;une r duction de leur contenu mitochondrial. Les mitochondries, lsquo;centrales lectriques rsquo; des cellules, sont cruciales pour la transmission synaptique. Nous montrons que deux souris mod les diff rents, de MA et de dysfonctionnement mitochondrial, pr sentent une alt ration pr coce des performances de m moire li es ces nouveaux neurones, qui ont une capacit synaptique r duite et moins de mitochondries. De plus, la manipulation g n tique des prog niteurs hippocampiques, chez le premier, r tablit les mitochondries et les synapses. Chez le second, l rsquo;exercice physique augmente les mitochondries et restaure les capacit s mn siques perdues.

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ABSTRACT
Some regions of the adult brain, such as the hippocampus, produce new neurons that participate in certain learning and memory capacities. In neurodegenerative diseases, such as Alzheimer 39 s AD , this adult neurogenesis is altered. In a mouse model of AD, we showed that these new neurons have a reduced mitochondrial content and less synaptic capacities. Mitochondria, 39 power plants 39 of cells, are particularly important in neurons and for synaptic transmission. We show that two different mouse models, of AD or of mitochondrial dysfunction, exhibit early impairment of memory performance related to these new neurons, which have less synaptic capacity and fewer mitochondria. In addition, we demonstrate that genetic manipulation of hippocampal progenitors in the former restores mitochondria and synapses. In the second, physical exercise increases mitochondria and restores lost memory abilities. Mitochondria are thus central in cognitive processes related to adult hippocampal neurogenesis.

Abstrak :
Penderita penyakit neurodegeneratif masih tinggi seiring pertambahan populasi manusia, diakibatkan oleh beberapa faktor seperti faktor lingkungan, neuroinflamasi, stress metabolik, neurovascular coupling dan genetik. Propolis telah banyak digunakan sebagai obat karena berbagai manfaatnya. Pada penelitian ini diteliti pengaruh propolis lebah yang tidak bersengat (Tetragonula sapiens) dari Sulawesi Selatan terhadap neurogenesis pada kultur primer embrio korteks serebri tikus Wistar dengan usia gestasi 17-18 hari. Penelitian ini merupakan penelitian eksperimental yang dibagi menjadi kelompok Kontrol, Vehicle dan kelompok yang diberikan ekstrak propolis. Penelitian ini diawali dengan pengujian MTS assay didapatkan dosis optimal, 0,5μg/mL dan 1μg/mL, lalu dilanjutkan pemeriksaan immunostaining menggunakan antibodi primer MAP (Microtubule-Associated Protein) 2 dan pemeriksaan ekspresi mRNA BDNF melalui qRT-PCR. Pada penelitian ini menunjukkan, propolis dapat meningkatkan viabilitas sel, merangsang pertumbuhan dendrit dan menghasilkan ekspresi mRNA BDNF (Brain Derived Neurotrophic Factor) yang signifikan dibandingkan kontrol. Hal ini menunjukkan propolis dapat menjadi kandidat penghambat pada penyakit neurodegeneratif. ......People with neurodegenerative disease is still high as the population increases, caused by several factors such as environmental factors, neuroinflammation, metabolic stress, neurovascular coupling and genetics. Propolis has been widely used as medicine due to its various benefits. This research investigated the effect of stingless bee propolis (Tetragonula sapiens) from South Sulawesi on neurogenesis in primary cultures of embryonic cerebral cortex of Wistar rats at 17-18 days of gestation. This research was an experimental study consisting of control group, vehicle group and propolis extract group. This research began with MTS assay testing to obtain the optimal dose, 0.5μg/mL and 1μg/mL, then continued with immunostaining examination using MAP (Microtubule-Associated Protein) 2 primary antibody and the examination of BDNF mRNA expression through qRT-PCR. The results showed that propolis can increase cell viability, stimulate dendrite growth and produce the expression of BDNF (Brain Derived Neurotrophic Factor) mRNA significantly higher than control. It is shown that propolis can be a candidate inhibitor in neurodegenerative diseases.

Abstrak :
Amyloid-forming proteins are implicated in over 30 human diseases. The proteins involved in each disease have unrelated sequences and dissimilar native structures, but they all undergo conformational alterations to form fibrillar polymers. The fibrillar assemblies accumulate progressively into disease-specific lesions in vivo. Substantial evidence suggests these lesions are the end state of aberrant protein folding whereas the actual disease-causing culprits likely are soluble, non-fibrillar assemblies preceding the aggregates. The non-fibrillar protein assemblies range from small, low-order oligomers to spherical, annular, and protofibrillar species. Oligomeric species are believed to mediate various pathogenic mechanisms that lead to cellular dysfunction, cytotoxicity, and cell loss, eventuating in disease-specific degeneration and systemic morbidity. The particular pathologies thus are determined by the afflicted cell types, organs, systems, and the proteins involved. Evidence suggests that the oligomeric species may share structural features and possibly common mechanisms of action. In many cases, the structure–function interrelationships amongst the various protein assemblies described in vitro are still elusive. Deciphering these intricate structure–function correlations will help understanding a complex array of pathogenic mechanisms, some of which may be common across different diseases albeit affecting different cell types and systems.

Abstrak :
Metal ions in the brain are a necessity as well as a poison. The presence of metal ions in the active sites of biological catalysts or metalloproteins and in the biological functioning of nucleic acids is very well documented and they are required for brain activity. On the other hand, metals are very effective in generating oxidative stress. This effect does not only play a role in immunology but also is the root of practically all neurodegenerative disorders by inducing disease via the death of neurons. Managing metal ions in the brain could therefore be an important strategy in the search for therapeutic agents used in the treatment of neurodegenerative diseases. This new title gives an overview to key topics in the area of metal ions in the brain. It focuses on the role of metal ions in neurological systems by describing their advantageous functions as well as their poisonous features. It is therefore of interest for scientists in biochemistry and biophysics, physiology, toxicology as well as for physicians focused on this topic.

Abstrak :
The editor of this volume, having research interests in the field of ROS production and the damage to cellular systems, has identified a number of enzymes showing ·OH scavenging activities details of which are anticipated to be published in the near future as confirmatory experiments are awaited. It is hoped that the information presented in this book on NDs will stimulate both expert and novice researchers in the field with excellent overviews of the current status of research and pointers to future research goals. Also the insights gained should be valuable for further understanding of the diseases at molecular levels and should lead to development of new biomarkers, novel diagnostic tools and more effective therapeutic drugs to treat the clinical problems raised by these devastating diseases.

Abstrak :
This book discusses the various methods to reprogram cells, the control and determination of cell identity, the epigenetic models that have emerged and the application of iPS cell therapy for brain diseases, in particular Parkinson’s disease and Vanishing White Matter (VWM).​

Abstrak :
As age related diseases increase in prevalence and impact more significantly on medical resources it is imperative to understand these diseases and the mechanisms behind their progression. New research has stimulated a growing interest in mitochondrial involvement in neurodegenerative disorders such as parkinson’s disease, alzheimer’s disease and multiple sclerosis and the mechanisms which lead from mitochondrial dysfunction to neurodegeneration. Mitochondrial dysfunction in neurodegenerative disorders brings together contributions from leaders in the field internationally on the various ways in which mitochondrial dysfunction contributes to the pathogenesis of these diseases, guiding the reader through the basic functions of mitochondria and the mechanisms that lead to their dysfunction, to the consequences of this dysfunction on neuronal function before finishing with the modelling of these disorders and discussion of new potential therapeutic targets.