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https://www.readbyqxmd.com/read/28822080/soluble-epoxide-hydrolase-inhibition-attenuates-mptp-induced-neurotoxicity-in-the-nigrostriatal-dopaminergic-system-involvement-of-%C3%AE-synuclein-aggregation-and-er-stress
#1
Hui-Ju Huang, Yi-Ting Wang, Hui-Ching Lin, Yi-Hsuan Lee, Anya Maan-Yuh Lin
Soluble epoxide hydrolase (sEH) is widely expressed in the mammalian brain and possesses dual enzymatic activities, including C-terminal epoxide hydrolase (C-EH) which degrades epoxyeicosatrienoic acid (EET), a beneficial arachidonic acid metabolite. In the present study, the neuroprotective effect of sEH inhibition on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurodegeneration of nigrostriatal dopaminergic system was investigated using genetic and pharmacological approaches. MPTP (15 mg/kg) was intraperitoneally injected in sEH knockout (KO) mice and C57BL/6J mice as wild-type (WT) mice...
August 18, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28821816/an-expandable-embryonic-stem-cell-derived-purkinje-neuron-progenitor-population-that-exhibits-in-vivo-maturation-in-the-adult-mouse-cerebellum
#2
Gustavo A Higuera, Grazia Iaffaldano, Meiwand Bedar, Guy Shpak, Robin Broersen, Shashini T Munshi, Catherine Dupont, Joost Gribnau, Femke M S de Vrij, Steven A Kushner, Chris I De Zeeuw
The directed differentiation of patient-derived induced pluripotent stem cells into cell-type specific neurons has inspired the development of therapeutic discovery for neurodegenerative diseases. Many forms of ataxia result from degeneration of cerebellar Purkinje cells, but thus far it has not been possible to efficiently generate Purkinje neuron (PN) progenitors from human or mouse pluripotent stem cells, let alone to develop a methodology for in vivo transplantation in the adult cerebellum. Here, we present a protocol to obtain an expandable population of cerebellar neuron progenitors from mouse embryonic stem cells...
August 18, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28821675/synergistic-toxicity-of-polyglutamine-expanded-tbp-in-glia-and-neuronal-cells-therapeutic-implications-for-sca17
#3
Yang Yang, Su Yang, Jifeng Guo, Yiting Cui, Baisha Tang, Xiao-Jiang Li, Shihua Li
Spinocerebellar ataxia 17 (SCA17) is caused by polyglutamine (polyQ) repeat expansion in the TATA-binding protein (TBP) and is among a family of neurodegenerative diseases in which polyQ expansion leads to preferential neuronal loss in the brain. Although previous studies have demonstrated that expression of polyQ-expanded proteins in glial cells can cause neuronal injury via non-cell-autonomous mechanisms, these studies investigated animal models that overexpress transgenic mutant proteins. Since glial cells are particularly reactive to overexpressed mutant proteins, it is important to investigate the in vivo role of glial dysfunction in neurodegeneration when mutant polyQ proteins are endogenously expressed...
August 18, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28821645/mutant-huntingtin-is-secreted-via-a-late-endosomal-lysosomal-unconventional-secretory-pathway
#4
Katarina Trajkovic, Hyunkyong Jeong, Dimitri Krainc
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by the expansion of a CAG triplet in the gene encoding for huntingtin. The resulting mutant protein huntingtin (mHtt) with extended polyglutamine (polyQ) sequence at the N-terminus leads to neuronal degeneration both in cell-autonomous and non-cell-autonomous manners. Recent studies identified mHtt in the extracellular environment and suggested that its spreading contributes to toxicity, but the mechanism of mHtt release from the cell of origin remains unknown...
August 16, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28821644/calpain-dependent-degradation-of-nucleoporins-contributes-to-motor-neuron-death-in-a-mouse-model-of-chronic-excitotoxicity
#5
Kaori Sugiyama, Tomomi Aida, Masatoshi Nomura, Ryoichi Takayanagi, Hanns U Zeilhofer, Kohichi Tanaka
Glutamate-mediated excitotoxicity induces neuronal death by altering various intracellular signaling pathways and is implicated as a common pathogenic pathway in many neurodegenerative diseases. In the case of motor neuron disease, there is significant evidence to suggest that overactivation of AMPA receptors due to deficiencies in the expression and function of glial glutamate transporter GLT1 and GLAST plays an important role in the mechanisms of neuronal death. However, a causal role for glial glutamate transporter dysfunction in motor neuron death remains unknown...
August 16, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28821643/changes-in-the-excitability-of-neocortical-neurons-in-a-mouse-model-of-amyotrophic-lateral-sclerosis-are-not-specific-to-corticospinal-neurons-and-are-modulated-by-advancing-disease
#6
Juhyun Kim, Ethan G Hughes, Ashwin S Shetty, Paola Arlotta, Loyal A Goff, Dwight E Bergles, Solange P Brown
Cell-type specific changes in neuronal excitability have been proposed to contribute to the selective degeneration of corticospinal neurons in amyotrophic lateral sclerosis (ALS) and to neocortical hyperexcitability, a prominent feature of both inherited and sporadic variants of the disease, but the mechanisms underlying selective loss of specific cell types in ALS are not known. We analyzed the physiological properties of distinct classes of cortical neurons in the motor cortex of hSOD1(G93A) mice of both sexes and found that they all exhibit increases in intrinsic excitability that depend on disease stage...
August 17, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28821446/diet-induced-obesity-alters-memory-consolidation-in-female-rats
#7
P Zanini, B D Arbo, G Niches, D Czarnabay, F Benetti, M F Ribeiro, A L Cecconello
Obesity is a multifactorial disease characterized by the abnormal or excessive fat accumulation, which is caused by an energy imbalance between consumed and expended calories. Obesity leads to an inflammatory response that may result in peripheral and central metabolic changes, including insulin and leptin resistance. Insulin and leptin resistance have been associated with metabolic and cognitive dysfunctions. Obesity and some neurodegenerative diseases that lead to dementia affect mainly women. However, the effects of diet-induced obesity on memory consolidation in female rats are poorly understood...
August 15, 2017: Physiology & Behavior
https://www.readbyqxmd.com/read/28820649/targets-of-neuroprotection-in-glaucoma
#8
Shaoqing He, Dorota L Stankowska, Dorette Z Ellis, Raghu R Krishnamoorthy, Thomas Yorio
Progressive neurodegeneration of the optic nerve and the loss of retinal ganglion cells is a hallmark of glaucoma, the leading cause of irreversible blindness worldwide, with primary open-angle glaucoma (POAG) being the most frequent form of glaucoma in the Western world. While some genetic mutations have been identified for some glaucomas, those associated with POAG are limited and for most POAG patients, the etiology is still unclear. Unfortunately, treatment of this neurodegenerative disease and other retinal degenerative diseases is lacking...
August 18, 2017: Journal of Ocular Pharmacology and Therapeutics
https://www.readbyqxmd.com/read/28820437/are-astrocytes-the-predominant-cell-type-for-activation-of-nrf2-in-aging-and-neurodegeneration
#9
REVIEW
Jeffrey R Liddell
Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that regulates hundreds of antioxidant genes, and is activated in response to oxidative stress. Given that many neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease and multiple sclerosis are characterised by oxidative stress, Nrf2 is commonly activated in these diseases. Evidence demonstrates that Nrf2 activity is repressed in neurons in vitro, and only cultured astrocytes respond strongly to Nrf2 inducers, leading to the interpretation that Nrf2 signalling is largely restricted to astrocytes...
August 18, 2017: Antioxidants (Basel, Switzerland)
https://www.readbyqxmd.com/read/28820184/age-related-macular-degeneration-and-mortality-the-melbourne-collaborative-cohort-study
#10
M B McGuinness, R P Finger, A Karahalios, R H Guymer, D R English, E W Chong, A M Hodge, L D Robman, G G Giles, J A Simpson
AimsTo assess associations between features of age-related macular degeneration (AMD) and mortality.MethodsA total of 21 129 participants from the Melbourne Collaborative Cohort Study aged 47-85 years (60% female) were assessed for AMD (2003-2007). Mortality data to December 31, 2012 were obtained through linkage with the National Death Index. Associations were assessed using Cox regression, adjusting for age, sex, smoking, region of birth, education, physical activity, diet and alcohol.ResultsLate AMD was identified in 122 (0...
August 18, 2017: Eye
https://www.readbyqxmd.com/read/28820054/qsar-modeling-of-histamine-h3r-antagonists-inverse-agonists-as-future-drugs-for-neurodegenerative-diseases
#11
Michelle Fidelis Corrêa, João Paulo Dos Santos Fernandes
Histamine H3 receptor (H3R) is associated with several neuropsychological diseases. It is predominantly expressed in the central nervous system as presynaptic receptor, especially in regions associated with cognition and behavior, and is responsible for modulate the synthesis and release of histamine and other neurotransmitters such as acetylcholine, dopamine and serotonin. Therefore, H3R is an important target involved in several CNS disorders, such as narcolepsy, attention deficit hyperactivity disorder and schizophrenia...
August 17, 2017: Current Neuropharmacology
https://www.readbyqxmd.com/read/28819888/paraquat-induced-movement-disorder-in-relation-to-oxidative-stress-mediated-neurodegeneration-in-the-brain-of-drosophila-melanogaster
#12
S Niveditha, S R Ramesh, T Shivanandappa
Exposure to pesticides like paraquat (PQ) is considered as a risk factor for Parkinson's disease (PD). PQ has been shown to induce PD-like phenotype in experimental animals. Drosophila, a valuable laboratory model organism, is widely used to study neurodegenerative disorders including PD. The acute (single dose) PQ model of PD in Drosophila is associated with high mortality as well as reversibility of locomotor deficits and, therefore, does not replicate the disease phenotype. We have investigated the relevance of the acute and multiple (sublethal) dose of PQ to induce PD-like symptoms in Drosophila and shown that multiple-dose of PQ induces irreversible locomotor impairment without significant mortality...
August 18, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28819795/leptin-regulation-of-synaptic-function-at-hippocampal-ta-ca1-and-sc-ca1-synapses-implications-for-health-and-disease
#13
Gemma McGregor, Jenni Harvey
Growing evidence indicates that the endocrine hormone leptin regulates hippocampal synaptic function in addition to its established role as a hypothalamic satiety signal. Indeed, numerous studies show that leptin facilitates the cellular events that underlie hippocampal learning and memory including activity-dependent synaptic plasticity and glutamate receptor trafficking, indicating that leptin may be a potential cognitive enhancer. Although there has been extensive investigation into the modulatory role of leptin at hippocampal Schaffer collateral (SC)-CA1 synapses, recent evidence indicates that leptin also potently regulates excitatory synaptic transmission at the anatomically distinct temporoammonic (TA) input to hippocampal CA1 neurons...
August 18, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28819135/ribosomal-transcription-is-regulated-by-pgc-1alpha-and-disturbed-in-huntington-s-disease
#14
Sarah Jesse, Hanna Bayer, Marius C Alupei, Martina Zügel, Medhanie Mulaw, Francesca Tuorto, Silke Malmsheimer, Karmveer Singh, Jürgen Steinacker, Uwe Schumann, Albert C Ludolph, Karin Scharffetter-Kochanek, Anke Witting, Patrick Weydt, Sebastian Iben
PGC-1α is a versatile inducer of mitochondrial biogenesis and responsive to the changing energy demands of the cell. As mitochondrial ATP production requires proteins that derive from translation products of cytosolic ribosomes, we asked whether PGC-1α directly takes part in ribosomal biogenesis. Here, we show that a fraction of cellular PGC-1α localizes to the nucleolus, the site of ribosomal transcription by RNA polymerase I. Upon activation PGC-1α associates with the ribosomal DNA and boosts recruitment of RNA polymerase I and UBF to the rDNA promoter...
August 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28819076/-molecularly-targeted-therapy-of-spinocerebellar-ataxia-type-1-by-hmgb1
#15
Kyota Fujita, Hitoshi Okazawa
Spinocerebellar ataxia type 1 (SCA1) is an untreatable neurodegenerative disease. We reported a decrease in HMGB1 levels in the nucleus of cerebellar neurons in mouse SCA 1. The decrease in this DNA architectural protein leads to the impairment of DNA repair and transcription, the two essential nuclear functions, and eventually causes neurodegeneration. We have designed a gene therapy using AAV-HMGB1 and tested it using the mouse model. Based on the results of these proof of concept (POC) studies, we are now preparing GMP-level AAV vector and designing human clinical trials...
August 2017: Brain and Nerve, Shinkei Kenkyū No Shinpo
https://www.readbyqxmd.com/read/28819072/-overview-of-hereditary-spinocerebellar-ataxias-in-japan
#16
Masayoshi Tada, Akio Yokoseki, Osamu Onodera
Hereditary spinocerebellar degenerations (SCD) are a group of neurodegenerative disorders characterized by slowly progressive ataxia associated with non-cerebellar neurological signs and symptoms. In the Japanese population, dominantly inherited SCDs are much more common than recessively inherited or X-linked SCDs. The most common dominantly inherited SCD in Japan, as well as in many other countries, is Machado-Joseph disease, also known as spinocerebellar ataxia type 3 (MJD/SCA3). MJD/SCA3 is frequently accompanied by non-cerebellar symptoms, including progressive external ophthalmoplegia, pyramidal signs, dystonia, rigidity, dysarthria, and distal muscle atrophies...
August 2017: Brain and Nerve, Shinkei Kenkyū No Shinpo
https://www.readbyqxmd.com/read/28819043/increased-acetylation-of-microtubules-rescues-human-tau-induced-microtubule-defects-and-neuromuscular-junction-abnormalities-in-drosophila
#17
Chuan-Xi Mao, Xue Wen, Shan Jin, Yong Q Zhang
Tau normally associates with and stabilizes microtubules (MTs), but is hyperphosphorylated and aggregated into neurofibrillary tangles in Alzheimer's disease and related neurodegenerative diseases, which are collectively known as tauopathies. MTs are regulated by different forms of post-translational modification including acetylation; acetylated MTs represent a more stable microtubule population. In our previous study, we show that inhibition of histone deacetylase 6 (HDAC6), which deacetylates tubulin at lysine 40, rescues defects in MTs and in neuromuscular junction growth caused by tau overexpression...
August 17, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/28818825/mr-imaging-features-of-the-cerebellum-in-adult-onset-neuronal-intranuclear-inclusion-disease-8-cases
#18
A Sugiyama, N Sato, Y Kimura, T Maekawa, M Enokizono, Y Saito, Y Takahashi, H Matsuda, S Kuwabara
Neuronal intranuclear inclusion disease is a neurodegenerative disorder pathologically characterized by eosinophilic hyaline intranuclear inclusions. A high-intensity signal along the corticomedullary junction on DWI has been described as a specific MR imaging finding of the cerebrum in neuronal intranuclear inclusion disease. However, MR imaging findings of the cerebellum in neuronal intranuclear inclusion disease have not been fully evaluated. Here, we review MR imaging findings of the cerebellum in a series of 8 patients with pathologically confirmed neuronal intranuclear inclusion disease...
August 17, 2017: AJNR. American Journal of Neuroradiology
https://www.readbyqxmd.com/read/28818116/distinct-white-matter-microstructural-abnormalities-and-extracellular-water-increases-relate-to-cognitive-impairment-in-alzheimer-s-disease-with-and-without-cerebrovascular-disease
#19
Fang Ji, Ofer Pasternak, Siwei Liu, Yng Miin Loke, Boon Linn Choo, Saima Hilal, Xin Xu, Mohammad Kamran Ikram, Narayanaswamy Venketasubramanian, Christopher Li-Hsian Chen, Juan Zhou
BACKGROUND: Mixed vascular and neurodegenerative dementia, such as Alzheimer's disease (AD) with concomitant cerebrovascular disease, has emerged as the leading cause of age-related cognitive impairment. The brain white matter (WM) microstructural changes in neurodegeneration well-documented by diffusion tensor imaging (DTI) can originate from brain tissue or extracellular free water changes. The differential microstructural and free water changes in AD with and without cerebrovascular disease, especially in normal-appearing WM, remain largely unknown...
August 17, 2017: Alzheimer's Research & Therapy
https://www.readbyqxmd.com/read/28817841/-practical-use-of-continuous-apomorphine-infusion-via-pump
#20
Lars Tönges, Andrés Ceballos-Baumann, Holger Honig, Alexander Storch, Wolfgang H Jost
Parkinson's disease is the second most common neurodegenerative illness after Alzheimer's disease. In its advanced stages, it is characterized by various special symptoms. In addition to non-motor signs, motor complications are most prominent and most often can only be inadequately improved with pulsatile oral therapies. However, with the aid of continuous dopaminergic stimulation, improvements can be achieved even in advanced stages of the disease. This will not only alleviate motor and non-motor symptoms, but will also lead to a better quality of life...
August 17, 2017: Fortschritte der Neurologie-Psychiatrie
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