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https://www.readbyqxmd.com/read/29759483/induction-of-the-immunoproteasome-subunit-lmp7-links-proteostasis-and-immunity-in-%C3%AE-synuclein-aggregation-disorders
#1
Scott Ugras, Malcolm J Daniels, Hossein Fazelinia, Neal S Gould, Anastasia K Yocum, Kelvin C Luk, Esteban Luna, Hua Ding, Chris McKennan, Steven Seeholzer, Dan Martinez, Perry Evans, Daniel Brown, John E Duda, Harry Ischiropoulos
Accumulation of aggregated α-synuclein into Lewy bodies is thought to contribute to the onset and progression of dopaminergic neuron degeneration in Parkinson's disease (PD) and related disorders. Although protein aggregation is associated with perturbation of proteostasis, how α-synuclein aggregation affects the brain proteome and signaling remains uncertain. In a mouse model of α-synuclein aggregation, 6% of 6215 proteins and 1.6% of 8183 phosphopeptides changed in abundance, indicating conservation of proteostasis and phosphorylation signaling...
May 11, 2018: EBioMedicine
https://www.readbyqxmd.com/read/29747690/a53t-%C3%AE-synuclein-overexpression-in-murine-locus-coeruleus-induces-parkinson-s-disease-like-pathology-in-neurons-and-glia
#2
Martin Timo Henrich, Fanni Fruzsina Geibl, Bolam Lee, Wei-Hua Chiu, James Benjamin Koprich, Jonathan Michael Brotchie, Lars Timmermann, Niels Decher, Lina Anita Matschke, Wolfgang Hermann Oertel
Degeneration of noradrenergic locus coeruleus neurons occurs during the prodromal phase of Parkinson's disease and contributes to a variety of non-motor symptoms, e.g. depression, anxiety and REM sleep behavior disorder. This study was designed to establish the first locus coeruleus α-synucleinopathy mouse model, which should provide sufficient information about the time-course of noradrenergic neurodegeneration, replicate cardinal histopathological features of the human Parkinson's disease neuropathology and finally lead to robust histological markers, which are sufficient to assess the pathological changes in a quantitative and qualitative way...
May 10, 2018: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/29729423/interaction-between-a-mapt-variant-causing-frontotemporal-dementia-and-mutant-app-affects-axonal-transport
#3
Robert Adalbert, Stefan Milde, Claire Durrant, Kunie Ando, Virginie Stygelbout, Zehra Yilmaz, Stacey Gould, Jean-Pierre Brion, Michael P Coleman
In Alzheimer's disease, many indicators point to a central role for poor axonal transport, but the potential for stimulating axonal transport to alleviate the disease remains largely untested. Previously, we reported enhanced anterograde axonal transport of mitochondria in 8- to 11-month-old MAPTP301L knockin mice, a genetic model of frontotemporal dementia with parkinsonism-17T. In this study, we further characterized the axonal transport of mitochondria in younger MAPTP301L mice crossed with the familial Alzheimer's disease model, TgCRND8, aiming to test whether boosting axonal transport in young TgCRND8 mice can alleviate axonal swelling...
April 5, 2018: Neurobiology of Aging
https://www.readbyqxmd.com/read/29700116/comparative-analysis-of-parkinson-s-disease-associated-genes-reveals-altered-survival-and-bioenergetics-of-parkin-deficient-dopamine-neurons-in-mice
#4
Nicolas Giguere, Consiglia Pacelli, Caroline Saumure, Marie-Josee Bourque, Diana Matheoud, Daniel Levesque, Ruth S Slack, David S Park, Louis-Eric Trudeau
Many mutations in genes encoding proteins such as parkin, PTEN-induced putative kinase 1 (PINK1), protein deglycase DJ-1 (DJ-1 or PARK7), leucine-rich repeat kinase 2 (LRRK2), and α-synuclein have been linked to familial forms of Parkinson's disease (PD). The consequences of these mutations, such as altered mitochondrial function and pathological protein aggregation, are starting to be better understood. However, little is known about the mechanisms explaining why alterations in such diverse cellular mechanisms lead to the selective loss of dopamine (DA) neurons in the substantia nigra (SNc) in the brain of individuals with PD...
April 26, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29688812/nitration-of-microtubules-blocks-axonal-mitochondrial-transport-in-a-human-pluripotent-stem-cell-model-of-parkinson-s-disease
#5
Morgan G Stykel, Kayla Humphries, Mathew P Kirby, Chris Czaniecki, Tinya Wang, Tammy Ryan, Vladimir Bamm, Scott D Ryan
Neuronal loss in Parkinson's disease (PD) is associated with aberrant mitochondrial function in dopaminergic (DA) neurons of the substantia nigra pars compacta. An association has been reported between PD onset and exposure to mitochondrial toxins, including the agrochemicals paraquat (PQ), maneb (MB), and rotenone (Rot). Here, with the use of a patient-derived stem cell model of PD, allowing comparison of DA neurons harboring a mutation in the α-synuclein (α-syn) gene ( SNCA-A53T) against isogenic, mutation-corrected controls, we describe a novel mechanism whereby NO, generated from SNCA-A53T mutant neurons exposed to Rot or PQ/MB, inhibits anterograde mitochondrial transport through nitration of α-tubulin (α-Tub)...
April 24, 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29649983/ncx-db-a-unified-resource-for-integrative-analysis-of-the-sodium-calcium-exchanger-super-family
#6
Katrin Bode, Damien M O'Halloran
Na+ /Ca2+ exchangers are low-affinity high-capacity transporters that mediate Ca2+ extrusion by coupling Ca2+ efflux to the influx of Na+ ions. The Na+ /Ca2+ exchangers form a super-family comprised of three branches each differing in ion-substrate selectivity: Na+ /Ca2+ exchangers (NCX), Na+ /Ca2+ /K+ exchangers, and Ca2+ /cation exchangers. Their primary function is to maintain Ca2+ homeostasis and play a particularly important role in excitable cells that experience transient Ca2+ fluxes. Research into the role and activity of Na+ /Ca2+ exchangers has focused extensively on the cardio-vascular system, however, growing evidence suggests that Na+ /Ca2+ exchangers play a key role in neuronal processes such as memory formation, learning, oligodendrocyte differentiation, neuroprotection during brain ischemia and axon guidance...
April 13, 2018: BMC Neuroscience
https://www.readbyqxmd.com/read/29548988/axonal-autophagy-mini-review-for-autophagy-in-the-cns
#7
REVIEW
Andrea K H Stavoe, Erika L F Holzbaur
Neurons are long-lived and highly polarized cells that depend on autophagy to maintain cellular homeostasis. The robust, constitutive biogenesis of autophagosomes in the distal axon occurs via a conserved pathway that is required to maintain functional synapses and prevent axon degeneration. Autophagosomes are formed de novo at the axon terminal in a stepwise assembly process, engulfing mitochondrial fragments, aggregated proteins, and bulk cytosol in what appears to be a nonselective uptake mechanism. Following formation, autophagosomes fuse with late endosomes/lysosomes and then are rapidly and efficiently transported along the axon toward the soma, driven by the microtubule motor cytoplasmic dynein...
March 13, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29463867/optogenetic-tractography-for-anatomo-functional-characterization-of-cortico-subcortical-neural-circuits-in-non-human-primates
#8
S Senova, C Poupon, J Dauguet, H J Stewart, G P Dugué, C Jan, K Hosomi, G S Ralph, L Barnes, X Drouot, C Pouzat, J F Mangin, F Pain, I Doignon, R Aron-Badin, E Brouillet, E S Boyden, K A Mitrophanous, P Hantraye, S Palfi
Dissecting neural circuitry in non-human primates (NHP) is crucial to identify potential neuromodulation anatomical targets for the treatment of pharmacoresistant neuropsychiatric diseases by electrical neuromodulation. How targets of deep brain stimulation (DBS) and cortical targets of transcranial magnetic stimulation (TMS) compare and might complement one another is an important question. Combining optogenetics and tractography may enable anatomo-functional characterization of large brain cortico-subcortical neural pathways...
February 20, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29436751/nigrostriatal-dopamine-transporter-availability-in-early-parkinson-s-disease
#9
Patrik Fazio, Per Svenningsson, Zsolt Cselényi, Christer Halldin, Lars Farde, Andrea Varrone
BACKGROUND: The imaging of biomarkers for characterization of dopaminergic impairment in Parkinson's disease (PD) is useful for diagnosis, patient stratification, and assessment of treatment outcomes. [18 F]FE-PE2I is an improved imaging tool allowing for detailed mapping of the dopamine transporter protein in the nigro-striatal system at the level of cell bodies (substantia nigra), axons, and presynaptic terminals (striatum). OBJECTIVES: The objective of this study was to compare the dopamine transporter protein loss in the presynaptic terminals to that in the cell bodies and axons in early PD patients using [18 F](E)-N-(3-iodoprop-2-enyl)-2b-carbofluoroethoxy-3b-(4'-methyl-phenyl) nortropane ([18 F]FE-PE2I) and high-resolution PET...
April 2018: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/29397556/whole-transcriptome-analysis-of-mouse-models-with-mptp-induced-early-stages-of-parkinson-s-disease-reveals-stage-specific-response-of-transcriptome-and-a-possible-role-of-myelin-linked-genes-in-neurodegeneration
#10
A Kh Alieva, V S Zyrin, M M Rudenok, A A Kolacheva, M V Shulskaya, M V Ugryumov, P A Slominsky, M I Shadrina
Parkinson's disease (PD) is characterized by degeneration of dopaminergic neurons. A whole-transcriptome analysis of the substantia nigra and striatum of an MPTP-induced mouse models of the earliest stages of PD was performed. Functional clustering of differentially represented transcripts revealed processes associated with the functioning of synapses, dendrites, axons, and myelination of neuronal projections. All of these processes occur in both the substantia nigra and striatum, but they are aimed at the functioning of neuron terminals in the striatum...
February 3, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29378186/effect-of-ghrelin-on-the-motor-deficit-caused-by-the-ablation-of-nigrostriatal-dopaminergic-cells-or-the-inhibition-of-striatal-dopamine-receptors
#11
Yukari Suda, Naoko Kuzumaki, Michiko Narita, Yusuke Hamada, Masahiro Shibasaki, Kenichi Tanaka, Hideki Tamura, Takashi Kawamura, Takashige Kondo, Akihiro Yamanaka, Minoru Narita
Ghrelin plays roles in a wide range of central functions by activating the growth hormone secretagogue receptor (GHSR). This receptor has recently been found in the substantia nigra (SN) to control dopamine (DA)-related physiological functions. The dysregulation of DA neurons in the SN pars compacta (SNc) and the consequent depletion of striatal DA are known to underlie the motor deficits observed in Parkinson's disease (PD). In the present study, we further investigated the role of the SN-ghrelin system in motor function under the stereotaxic injection of AAV-CMV-FLEX-diphtheria toxin A (DTA) into the SN of dopamine transporter (DAT)-Cre (DATSN ::DTA) mice to expunge DA neurons of the SNc...
February 19, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29360949/dopaminergic-abnormalities-following-traumatic-brain-injury
#12
Peter O Jenkins, Sara De Simoni, Niall J Bourke, Jessica Fleminger, Gregory Scott, David J Towey, William Svensson, Sameer Khan, Maneesh Patel, Richard Greenwood, James H Cole, David J Sharp
Traumatic brain injury can reduce striatal dopamine levels. The cause of this is uncertain, but is likely to be related to damage to the nigrostriatal system. We investigated the pattern of striatal dopamine abnormalities using 123I-Ioflupane single-photon emission computed tomography (SPECT) scans and their relationship to nigrostriatal damage and clinical features. We studied 42 moderate-severe traumatic brain injury patients with cognitive impairments but no motor parkinsonism signs and 20 healthy controls...
January 17, 2018: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29337233/tau-deficiency-down-regulated-transcription-factor-orthodenticle-homeobox-2-expression-in-the-dopaminergic-neurons-in-ventral-tegmental-area-and-caused-no-obvious-motor-deficits-in-mice
#13
Xiaolu Tang, Luyan Jiao, Meige Zheng, Yan Yan, Qi Nie, Ting Wu, Xiaomei Wan, Guofeng Zhang, Yonglin Li, Song Wu, Bin Jiang, Huaibin Cai, Pingyi Xu, Jinhai Duan, Xian Lin
Tau protein participates in microtubule stabilization, axonal transport, and protein trafficking. Loss of normal tau function will exert a negative effect. However, current knowledge on the impact of tau deficiency on the motor behavior and related neurobiological changes is controversial. In this study, we examined motor functions and analyzed several proteins implicated in the maintenance of midbrain dopaminergic (DA) neurons (mDANs) function of adult and aged tau+/+ , tau+/- , tau-/- mice. We found tau deficiency could not induce significant motor disorders...
March 1, 2018: Neuroscience
https://www.readbyqxmd.com/read/29180624/alpha-synuclein-facilitates-to-form-short-unconventional-microtubules-that-have-a-unique-function-in-the-axonal-transport
#14
Shiori Toba, Mingyue Jin, Masami Yamada, Kanako Kumamoto, Sakiko Matsumoto, Takuo Yasunaga, Yuko Fukunaga, Atsuo Miyazawa, Sakiko Fujita, Kyoko Itoh, Shinji Fushiki, Hiroaki Kojima, Hideki Wanibuchi, Yoshiyuki Arai, Takeharu Nagai, Shinji Hirotsune
Although α-synuclein (αSyn) has been linked to Parkinson's disease (PD), the mechanisms underlying the causative role in PD remain unclear. We previously proposed a model for a transportable microtubule (tMT), in which dynein is anchored to a short tMT by LIS1 followed by the kinesin-dependent anterograde transport; however the mechanisms that produce tMTs have not been determined. Our in vitro investigations of microtubule (MT) dynamics revealed that αSyn facilitates the formation of short MTs and preferentially binds to MTs carrying 14 protofilaments (pfs)...
November 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29056362/critical-appraisal-of-pathology-transmission-in-the-%C3%AE-synuclein-fibril-model-of-lewy-body-disorders
#15
Negin Nouraei, Daniel M Mason, Kristin M Miner, Michael A Carcella, Tarun N Bhatia, Benjamin K Dumm, Dishaben Soni, David A Johnson, Kelvin C Luk, Rehana K Leak
Lewy body disorders are characterized by the emergence of α-synucleinopathy in many parts of the central and peripheral nervous systems, including in the telencephalon. Dense α-synuclein+ pathology appears in regio inferior of the hippocampus in both Parkinson's disease and dementia with Lewy bodies and may disturb cognitive function. The preformed α-synuclein fibril model of Parkinson's disease is growing in use, given its potential for seeding the self-propagating spread of α-synucleinopathy throughout the mammalian brain...
January 2018: Experimental Neurology
https://www.readbyqxmd.com/read/29035751/intercellular-transfer-of-pathogenic-%C3%AE-synuclein-by-extracellular-vesicles-is-induced-by-the-lipid-peroxidation-product-4-hydroxynonenal
#16
Shi Zhang, Erez Eitan, Tsung-Yu Wu, Mark P Mattson
Parkinson's disease (PD) is characterized by accumulations of toxic α-synuclein aggregates in vulnerable neuronal populations in the brainstem, midbrain, and cerebral cortex. Recent findings suggest that α-synuclein pathology can be propagated transneuronally, but the underlying molecular mechanisms are unknown. Advances in the genetics of rare early-onset familial PD indicate that increased production and/or reduced autophagic clearance of α-synuclein can cause PD. The cause of the most common late-onset PD is unclear, but may involve metabolic compromise and oxidative stress upstream of α-synuclein accumulation...
January 2018: Neurobiology of Aging
https://www.readbyqxmd.com/read/28977448/optic-neuropathies-the-tip-of-the-neurodegeneration-iceberg
#17
REVIEW
Valerio Carelli, Chiara La Morgia, Fred N Ross-Cisneros, Alfredo A Sadun
The optic nerve and the cells that give origin to its 1.2 million axons, the retinal ganglion cells (RGCs), are particularly vulnerable to neurodegeneration related to mitochondrial dysfunction. Optic neuropathies may range from non-syndromic genetic entities, to rare syndromic multisystem diseases with optic atrophy such as mitochondrial encephalomyopathies, to age-related neurodegenerative diseases such as Alzheimer's and Parkinson's disease where optic nerve involvement has, until recently, been a relatively overlooked feature...
October 1, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28816642/proteomic-analysis-of-the-human-olfactory-bulb
#18
Manjunath Dammalli, Gourav Dey, Anil K Madugundu, Manish Kumar, Benvil Rodrigues, Harsha Gowda, Bychapur Gowrishankar Siddaiah, Anita Mahadevan, Susarla Krishna Shankar, Thottethodi Subrahmanya Keshava Prasad
The importance of olfaction to human health and disease is often underappreciated. Olfactory dysfunction has been reported in association with a host of common complex diseases, including neurological diseases such as Alzheimer's disease and Parkinson's disease. For health, olfaction or the sense of smell is also important for most mammals, for optimal engagement with their environment. Indeed, animals have developed sophisticated olfactory systems to detect and interpret the rich information presented to them to assist in day-to-day activities such as locating food sources, differentiating food from poisons, identifying mates, promoting reproduction, avoiding predators, and averting death...
August 2017: Omics: a Journal of Integrative Biology
https://www.readbyqxmd.com/read/28743955/early-synaptic-dysfunction-induced-by-%C3%AE-synuclein-in-a-rat-model-of-parkinson-s-disease
#19
Jenny-Ann Phan, Kathrine Stokholm, Justyna Zareba-Paslawska, Steen Jakobsen, Kim Vang, Albert Gjedde, Anne M Landau, Marina Romero-Ramos
Evidence suggests that synapses are affected first in Parkinson's disease (PD). Here, we tested the claim that pathological accumulation of α-synuclein, and subsequent synaptic disruption, occur in absence of dopaminergic neuron loss in PD. We determined early synaptic changes in rats that overexpress human α-synuclein by local injection of viral-vectors in midbrain. We aimed to achieve α-synuclein levels sufficient to induce terminal pathology without significant loss of nigral neurons. We tested synaptic disruption in vivo by analyzing motor defects and binding of a positron emission tomography (PET) radioligand to the vesicular monoamine transporter 2, (VMAT2), [(11)C]dihydrotetrabenazine (DTBZ)...
July 25, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28706191/aldehyde-dehydrogenase-1-positive-nigrostriatal-dopaminergic-fibers-exhibit-distinct-projection-pattern-and-dopamine-release-dynamics-at-mouse-dorsal-striatum
#20
Carmelo Sgobio, Junbing Wu, Wang Zheng, Xi Chen, Jing Pan, Armando G Salinas, Margaret I Davis, David M Lovinger, Huaibin Cai
Aldehyde dehydrogenase 1 (ALDH1A1)-positive dopaminergic (DA) neurons at the ventral substantia nigra pars compacta (SNpc) preferentially degenerate in Parkinson's disease (PD). Their projection pattern and dopamine release properties, however, remains uncharacterized. Here we show that ALDH1A1-positive axons project predominantly to the rostral two-thirds of dorsal striatum. A portion of these axons converge on a small fraction of striosome compartments restricted to the dorsolateral striatum (DLS), where less dopamine release was measured compared to the adjacent matrix enriched with the ALDH1A1-negative axons...
July 13, 2017: Scientific Reports
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