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https://www.readbyqxmd.com/read/28086964/anti-%C3%AE-synuclein-immunotherapy-reduces-%C3%AE-synuclein-propagation-in-the-axon-and-degeneration-in-a-combined-viral-vector-and-transgenic-model-of-synucleinopathy
#1
Brian Spencer, Elvira Valera, Edward Rockenstein, Cassia Overk, Michael Mante, Anthony Adame, Wagner Zago, Peter Seubert, Robin Barbour, Dale Schenk, Dora Games, Robert A Rissman, Eliezer Masliah
Neurodegenerative disorders such as Parkinson's Disease (PD), PD dementia (PDD) and Dementia with Lewy bodies (DLB) are characterized by progressive accumulation of α-synuclein (α-syn) in neurons. Recent studies have proposed that neuron-to-neuron propagation of α-syn plays a role in the pathogenesis of these disorders. We have previously shown that antibodies against the C-terminus of α-syn reduce the intra-neuronal accumulation of α-syn and related deficits in transgenic models of synucleinopathy, probably by abrogating the axonal transport and accumulation of α-syn in in vivo models...
January 13, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28012891/altered-microtubule-dynamics-in-neurodegenerative-disease-therapeutic-potential-of-microtubule-stabilizing-drugs
#2
Kurt R Brunden, Virginia M-Y Lee, Amos B Smith, John Q Trojanowski, Carlo Ballatore
Many neurodegenerative diseases are characterized by deficiencies in neuronal axonal transport, a process in which cellular cargo is shuttled with the aid of molecular motors from the cell body to axonal termini and back along microtubules (MTs). Proper axonal transport is critical to the normal functioning of neurons, and impairments in this process could contribute to the neuronal damage and death that is characteristic of neurodegenerative disease. Although the causes of axonal transport abnormalities may vary among the various neurodegenerative conditions, in many cases it appears that the transport deficiencies result from a diminution of axonal MT stability...
December 22, 2016: Neurobiology of Disease
https://www.readbyqxmd.com/read/28004277/tauroursodeoxycholic-bile-acid-arrests-axonal-degeneration-by-inhibiting-the-unfolded-protein-response-in-x-linked-adrenoleukodystrophy
#3
Nathalie Launay, Montserrat Ruiz, Laia Grau, Francisco J Ortega, Ekaterina V Ilieva, Juan José Martínez, Elena Galea, Isidre Ferrer, Erwin Knecht, Aurora Pujol, Stéphane Fourcade
The activation of the highly conserved unfolded protein response (UPR) is prominent in the pathogenesis of the most prevalent neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), which are classically characterized by an accumulation of aggregated or misfolded proteins. This activation is orchestrated by three endoplasmic reticulum (ER) stress sensors: PERK, ATF6 and IRE1. These sensors transduce signals that induce the expression of the UPR gene programme...
February 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/27956085/effects-of-%C3%AE-synuclein-on-axonal-transport
#4
Laura A Volpicelli-Daley
Lewy bodies and Lewy neurites composed primarily of α-synuclein characterize synucleinopathies including Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB). Despite decades of research on the impact of α-synuclein, little is known how abnormal inclusion made of this protein compromise neuronal function. Emerging evidence suggests that defects in axonal transport caused by aggregated α-synuclein contribute to neuronal dysfunction. These defects appear to occur well before the onset of neuronal death...
December 9, 2016: Neurobiology of Disease
https://www.readbyqxmd.com/read/27830778/defects-in-trafficking-bridge-parkinson-s-disease-pathology-and-genetics
#5
REVIEW
Asa Abeliovich, Aaron D Gitler
Parkinson's disease is a debilitating, age-associated movement disorder. A central aspect of the pathophysiology of Parkinson's disease is the progressive demise of midbrain dopamine neurons and their axonal projections, but the underlying causes of this loss are unclear. Advances in genetics and experimental model systems have illuminated an important role for defects in intracellular transport pathways to lysosomes. The accumulation of altered proteins and damaged mitochondria, particularly at axon terminals, ultimately might overwhelm the capacity of intracellular disposal mechanisms...
10, 2016: Nature
https://www.readbyqxmd.com/read/27757833/microtubule-destabilization-paves-the-way-to-parkinson-s-disease
#6
D Cartelli, G Cappelletti
Microtubules are dynamic structures normally associated to the cell division, during which they form the mitotic spindle, as well as to the initial phases of specification and polarization of various cell types, including neurons. Although microtubules could have a role in the death of many cells and tissues, the microtubule-based degenerative mechanisms have been poorly investigated; nevertheless, during the last two decades, many clues have been accumulated suggesting the importance of the microtubule system during neurodegeneration...
October 18, 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/27641766/mitochondrial-dynamics-in-visual-cortex-are-limited-in-vivo-and-not-affected-by-axonal-structural-plasticity
#7
Laura Smit-Rigter, Rajeev Rajendran, Catia A P Silva, Liselot Spierenburg, Femke Groeneweg, Emma M Ruimschotel, Danielle van Versendaal, Chris van der Togt, Ulf T Eysel, J Alexander Heimel, Christian Lohmann, Christiaan N Levelt
Mitochondria buffer intracellular Ca(2+) and provide energy [1]. Because synaptic structures with high Ca(2+) buffering [2-4] or energy demand [5] are often localized far away from the soma, mitochondria are actively transported to these sites [6-11]. Also, the removal and degradation of mitochondria are tightly regulated [9, 12, 13], because dysfunctional mitochondria are a source of reactive oxygen species, which can damage the cell [14]. Deficits in mitochondrial trafficking have been proposed to contribute to the pathogenesis of Parkinson's disease, schizophrenia, amyotrophic lateral sclerosis, optic atrophy, and Alzheimer's disease [13, 15-19]...
October 10, 2016: Current Biology: CB
https://www.readbyqxmd.com/read/27497486/is-axonal-degeneration-a-key-early-event-in-parkinson-s-disease
#8
Zuzanna Kurowska, Jeffrey H Kordower, A Jon Stoessl, Robert E Burke, Patrik Brundin, Zhenyu Yue, Scott T Brady, Jeffrey Milbrandt, Bruce D Trapp, Todd B Sherer, Satish Medicetty
Recent research suggests that in Parkinson's disease the long, thin and unmyelinated axons of dopaminergic neurons degenerate early in the disease process. We organized a workshop entitled 'Axonal Pathology in Parkinson's disease', on March 23rd, 2016, in Cleveland, Ohio with the goals of summarizing the state-of-the-art and defining key gaps in knowledge. A group of eight research leaders discussed new developments in clinical pathology, functional imaging, animal models, and mechanisms of degeneration including neuroinflammation, autophagy and axonal transport deficits...
October 19, 2016: Journal of Parkinson's Disease
https://www.readbyqxmd.com/read/27452482/live-imaging-of-mitochondrial-dynamics-in-cns-dopaminergic-neurons-in-vivo-demonstrates-early-reversal-of-mitochondrial-transport-following-mpp-exposure
#9
April A Dukes, Qing Bai, Victor S Van Laar, Yangzhong Zhou, Vladimir Ilin, Christopher N David, Zeynep S Agim, Joshua L Bonkowsky, Jason R Cannon, Simon C Watkins, Claudette M St Croix, Edward A Burton, Sarah B Berman
Extensive convergent evidence collectively suggests that mitochondrial dysfunction is central to the pathogenesis of Parkinson's disease (PD). Recently, changes in the dynamic properties of mitochondria have been increasingly implicated as a key proximate mechanism underlying neurodegeneration. However, studies have been limited by the lack of a model in which mitochondria can be imaged directly and dynamically in dopaminergic neurons of the intact vertebrate CNS. We generated transgenic zebrafish in which mitochondria of dopaminergic neurons are labeled with a fluorescent reporter, and optimized methods allowing direct intravital imaging of CNS dopaminergic axons and measurement of mitochondrial transport in vivo...
November 2016: Neurobiology of Disease
https://www.readbyqxmd.com/read/27413149/compartmentalized-regulation-of-parkin-mediated-mitochondrial-quality-control-in-the-drosophila-nervous-system-in-vivo
#10
Hyun Sung, Lauren C Tandarich, Kenny Nguyen, Peter J Hollenbeck
UNLABELLED: In neurons, the normal distribution and selective removal of mitochondria are considered essential for maintaining the functions of the large asymmetric cell and its diverse compartments. Parkin, a E3 ubiquitin ligase associated with familial Parkinson's disease, has been implicated in mitochondrial dynamics and removal in cells including neurons. However, it is not clear how Parkin functions in mitochondrial turnover in vivo, or whether Parkin-dependent events of the mitochondrial life cycle occur in all neuronal compartments...
July 13, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27193205/early-synaptic-dysfunction-in-parkinson-s-disease-insights-from-animal-models
#11
REVIEW
Tommaso Schirinzi, Graziella Madeo, Giuseppina Martella, Marta Maltese, Barbara Picconi, Paolo Calabresi, Antonio Pisani
The appearance of motor manifestations in Parkinson's disease (PD) is invariably linked to degeneration of nigral dopaminergic neurons of the substantia nigra pars compacta. Traditional views on PD neuropathology have been grounded in the assumption that the prime event of neurodegeneration involves neuronal cell bodies with the accumulation of metabolic products. However, this view has recently been challenged by both clinical and experimental evidence. Neuropathological studies in human brain samples and both in vivo and in vitro models support the hypothesis that nigrostriatal synapses may indeed be affected at the earliest stages of the neurodegenerative process...
June 2016: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/27148685/distal-retinal-ganglion-cell-axon-transport-loss-and-activation-of-p38-mapk-stress-pathway-following-vegf-a-antagonism
#12
R Foxton, A Osborne, K R Martin, Y-S Ng, D T Shima
There is increasing evidence that VEGF-A antagonists may be detrimental to neuronal health following ocular administration. Here we investigated firstly the effects of VEGF-A neutralization on retinal neuronal survival in the Ins2(Akita) diabetic and JR5558 spontaneous choroidal neovascularization (CNV) mice, and then looked at potential mechanisms contributing to cell death. We detected elevated apoptosis in the ganglion cell layer in both these models following VEGF-A antagonism, indicating that even when vascular pathologies respond to treatment, neurons are still vulnerable to reduced VEGF-A levels...
May 5, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27095262/the-cytoskeleton-as-a-novel-therapeutic-target-for-old-neurodegenerative-disorders
#13
REVIEW
Jessica Eira, Catarina Santos Silva, Mónica Mendes Sousa, Márcia Almeida Liz
Cytoskeleton defects, including alterations in microtubule stability, in axonal transport as well as in actin dynamics, have been characterized in several unrelated neurodegenerative conditions. These observations suggest that defects of cytoskeleton organization may be a common feature contributing to neurodegeneration. In line with this hypothesis, drugs targeting the cytoskeleton are currently being tested in animal models and in human clinical trials, showing promising effects. Drugs that modulate microtubule stability, inhibitors of posttranslational modifications of cytoskeletal components, specifically compounds affecting the levels of tubulin acetylation, and compounds targeting signaling molecules which regulate cytoskeleton dynamics, constitute the mostly addressed therapeutic interventions aiming at preventing cytoskeleton damage in neurodegenerative disorders...
June 2016: Progress in Neurobiology
https://www.readbyqxmd.com/read/27078024/progressive-axonal-degeneration-of-nigrostriatal-dopaminergic-neurons-in-calcium-independent-phospholipase-a2%C3%AE-knockout-mice
#14
Goichi Beck, Koei Shinzawa, Hideki Hayakawa, Kousuke Baba, Hisae Sumi-Akamaru, Yoshihide Tsujimoto, Hideki Mochizuki
Calcium-independent phospholipase A2β (iPLA2β, PLA2G6) is essential for the remodeling of membrane glycerophospholipids. Mutations in this gene are responsible for autosomal recessive, young onset, L-dopa-responsive parkinsonism (PARK14), suggesting a neurodegenerative condition in the nigrostriatal dopaminergic system in patients with PLA2G6 mutations. We previously observed slowly progressive motor deficits in iPLA2β-knockout (KO) mice. To clarify whether a deficiency of iPLA2β leads to the degeneration of nigrostriatal dopaminergic neurons, we analyzed the striatum of iPLA2β-KO mice...
2016: PloS One
https://www.readbyqxmd.com/read/27014695/dietary-plant-lectins-appear-to-be-transported-from-the-gut-to-gain-access-to-and-alter-dopaminergic-neurons-of-caenorhabditis-elegans-a-potential-etiology-of-parkinson-s-disease
#15
Jolene Zheng, Mingming Wang, Wenqian Wei, Jeffrey N Keller, Binita Adhikari, Jason F King, Michael L King, Nan Peng, Roger A Laine
Lectins from dietary plants have been shown to enhance drug absorption in the gastrointestinal tract of rats, be transported trans-synaptically as shown by tracing of axonal and dendritic paths, and enhance gene delivery. Other carbohydrate-binding protein toxins are known to traverse the gut intact in dogs. Post-feeding rhodamine- or TRITC-tagged dietary lectins, the lectins were tracked from gut to dopaminergic neurons (DAergic-N) in transgenic Caenorhabditis elegans (C. elegans) [egIs1(Pdat-1:GFP)] where the mutant has the green fluorescent protein (GFP) gene fused to a dopamine transport protein gene labeling DAergic-N...
2016: Frontiers in Nutrition
https://www.readbyqxmd.com/read/27003787/alterations-in-activity-dependent-neuroprotective-protein-in-sporadic-and-experimental-parkinson-s-disease
#16
Yaping Chu, Gerardo A Morfini, Jeffrey H Kordower
BACKGROUND: Activity-dependent neuroprotective protein (ADNP) is essential for brain formation and neuronal survival. It is possible that intracellular alpha-synuclein (α-syn) inclusions may be due to, or may cause, down-regulation of ADNP expression. OBJECTIVE: This study were to determine whether ADNP protein levels are altered in nigral dopaminergic neurons, establish whether ADNP alterations are associated with α-syn accumulation, and evaluate potential correlations between levels of ADNP expression and axonal transport motor proteins in sporadic and experimental Parkinson's disease (PD)...
2016: Journal of Parkinson's Disease
https://www.readbyqxmd.com/read/26877087/the-neuronal-kinesin-unc-104-kif1a-is-a-key-regulator-of-synaptic-aging-and-insulin-signaling-regulated-memory
#17
Ling-Bo Li, Haoyun Lei, Rachel N Arey, Pengpeng Li, Jianfeng Liu, Coleen T Murphy, X Z Shawn Xu, Kang Shen
Aging is the greatest risk factor for a number of neurodegenerative diseases, such as Alzheimer's and Parkinson's disease. Furthermore, normal aging is associated with a decline in sensory, motor, and cognitive functions. Emerging evidence suggests that synapse alterations, rather than neuronal cell death, are the causes of neuronal dysfunctions in normal aging and in early stages of neurodegenerative diseases. However, little is known about the mechanisms underlying age-related synaptic decline. Here, we uncover a surprising role of the anterograde molecular motor UNC-104/KIF1A as a key regulator of neural circuit deterioration in aging C...
March 7, 2016: Current Biology: CB
https://www.readbyqxmd.com/read/26853528/chaperone-complex-bag2-hsc70-regulates-localization-of-caenorhabditis-elegans-leucine-rich-repeat-kinase-lrk-1-to-the-golgi
#18
Takashi Fukuzono, Strahil Iv Pastuhov, Okinobu Fukushima, Chun Li, Ayuna Hattori, Shun-ichiro Iemura, Tohru Natsume, Hiroshi Shibuya, Hiroshi Hanafusa, Kunihiro Matsumoto, Naoki Hisamoto
Mutations in LRRK2 are linked to autosomal dominant forms of Parkinson's disease. We identified two human proteins that bind to LRRK2: BAG2 and HSC70, which are known to form a chaperone complex. We characterized the role of their Caenorhabditis elegans homologues, UNC-23 and HSP-1, in the regulation of LRK-1, the sole homologue of human LRRK2. In C. elegans, LRK-1 determines the polarized sorting of synaptic vesicle (SV) proteins to the axons by excluding SV proteins from the dendrite-specific transport machinery in the Golgi...
April 2016: Genes to Cells: Devoted to Molecular & Cellular Mechanisms
https://www.readbyqxmd.com/read/26844571/ampk-as-a-new-attractive-therapeutic-target-for-disease-prevention-the-role-of-dietary-compounds-ampk-and-disease-prevention
#19
Massimiliano Gasparrini, Francesca Giampieri, Josè Alvarez Suarez, Luca Mazzoni, Tamara Y Forbes Hernandez, Josè L Quiles, Pedro Bullon, Maurizio Battino
AMPK is a serine/threonine protein kinase that has the function of maintaining the balance between ATP production and consumption in most eukaryotic cells. It plays a relevant role in regulating cellular metabolism, preserving cellular energy homeostasis, and is involved in many other cellular processes as well as metabolic ones, including cell cycle regulation and endothelial and vascular relaxation. Recently, the effects of naturally occurring compounds able to prevent and treat diseases through AMPK activation have attracted the attention of many researchers...
2016: Current Drug Targets
https://www.readbyqxmd.com/read/26820848/axonal-transport-and-secretion-of-fibrillar-forms-of-%C3%AE-synuclein-a%C3%AE-42-peptide-and-httexon-1
#20
Michel Brahic, Luc Bousset, Gregor Bieri, Ronald Melki, Aaron D Gitler
Accruing evidence suggests that prion-like behavior of fibrillar forms of α-synuclein, β-amyloid peptide and mutant huntingtin are responsible for the spread of the lesions that characterize Parkinson disease, Alzheimer disease and Huntington disease, respectively. It is unknown whether these distinct protein assemblies are transported within and between neurons by similar or distinct mechanisms. It is also unclear if neuronal death or injury is required for neuron-to-neuron transfer. To address these questions, we used mouse primary cortical neurons grown in microfluidic devices to measure the amounts of α-synuclein, Aβ42 and HTTExon1 fibrils transported by axons in both directions (anterograde and retrograde), as well as to examine the mechanism of their release from axons after anterograde transport...
April 2016: Acta Neuropathologica
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