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Neurodegenerative disease

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https://www.readbyqxmd.com/read/28549134/transdiagnostic-neurology-neuropsychiatric-symptoms-in-neurodegenerative-diseases
#1
Masud Husain
No abstract text is available yet for this article.
June 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28549128/atad3-gene-cluster-deletions-cause-cerebellar-dysfunction-associated-with-altered-mitochondrial-dna-and-cholesterol-metabolism
#2
Radha Desai, Ann E Frazier, Romina Durigon, Harshil Patel, Aleck W Jones, Ilaria Dalla Rosa, Nicole J Lake, Alison G Compton, Hayley S Mountford, Elena J Tucker, Alice L R Mitchell, Deborah Jackson, Abdul Sesay, Miriam Di Re, Lambert P van den Heuvel, Derek Burke, David Francis, Sebastian Lunke, George McGillivray, Simone Mandelstam, Fanny Mochel, Boris Keren, Claude Jardel, Anne M Turner, P Ian Andrews, Jan Smeitink, Johannes N Spelbrink, Simon J Heales, Masakazu Kohda, Akira Ohtake, Kei Murayama, Yasushi Okazaki, Anne Lombès, Ian J Holt, David R Thorburn, Antonella Spinazzola
Although mitochondrial disorders are clinically heterogeneous, they frequently involve the central nervous system and are among the most common neurogenetic disorders. Identifying the causal genes has benefited enormously from advances in high-throughput sequencing technologies; however, once the defect is known, researchers face the challenge of deciphering the underlying disease mechanism. Here we characterize large biallelic deletions in the region encoding the ATAD3C, ATAD3B and ATAD3A genes. Although high homology complicates genomic analysis of the ATAD3 defects, they can be identified by targeted analysis of standard single nucleotide polymorphism array and whole exome sequencing data...
June 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28548540/nicotinamide-adenine-dinucleotide-nad-sup-sup-metabolism-and-neurodegeneration
#3
Mariana Pehar, Benjamin A Harlan, Kelby M Killoy, Marcelo R Vargas
SIGNIFICANCE: Nicotinamide adenine dinucleotide (NAD<sup>+</sup>) participates in redox reactions and NAD<sup>+</sup>-dependent signaling processes, which involve the cleavage of NAD<sup>+</sup> coupled to post-translational modifications of proteins or the production of second messengers. Either as a primary cause or as a secondary component of the pathogenic process, mitochondrial dysfunction and oxidative stress are prominent features of several neurodegenerative diseases...
May 26, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28546318/an-environment-dependent-transcriptional-network-specifies-human-microglia-identity
#4
David Gosselin, Dylan Skola, Nicole G Coufal, Inge R Holtman, Johannes C M Schlachetzki, Eniko Sajti, Baptiste N Jaeger, Carolyn O'Connor, Conor Fitzpatrick, Martina P Pasillas, Monique Pena, Amy Adair, David G Gonda, Michael L Levy, Richard M Ransohoff, Fred H Gage, Christopher K Glass
Microglia play essential roles in central nervous system (CNS) homeostasis and influence diverse aspects of neuronal function. However, the transcriptional mechanisms that specify human microglia phenotypes are largely unknown. We examined the transcriptomes and epigenetic landscapes of human microglia isolated from surgically resected brain tissue ex vivo and following transition to an in vitro environment. Transfer to a tissue culture environment results in rapid and extensive downregulation of microglia-specific genes that are induced in primitive mouse macrophages following migration into the fetal brain...
May 25, 2017: Science
https://www.readbyqxmd.com/read/28546289/a-tripeptidyl-peptidase-1-is-a-binding-partner-of-gphr-golgi-ph-regulator-in-dictyostelium
#5
Maria Stumpf, Rolf Müller, Berthold Gaßen, Regina Wehrstedt, Petra Fey, Malte A Karow, Ludwig Eichinger, Gernot Glöckner, Angelika A Noegel
Mutations in tripeptidyl peptidase 1 (TPP1) have been associated with late infantile neuronal ceroid lipofuscinosis (NCL2), a neurodegenerative disorder. TPP1 is a lysosomal serine protease, which removes tripeptides from the amino terminus of proteins and is composed of an N-terminal prodomain and a catalytic domain. It is conserved in mammals, amphibians, fish and the amoeba Dictyostelium discoideum. D. discoideum harbors at least six genes encoding tripeptidyl peptidase 1, tpp1A to tpp1F We identified TPP1F as binding partner of Dictyostelium GPHR (Golgi pH regulator), which is an evolutionary highly conserved intracellular transmembrane protein...
May 25, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/28545972/lithium-alleviates-neurotoxic-prion-peptide-induced-synaptic-damage-and-neuronal-death-partially-by-the-upregulation-of-nuclear-target-rest-and-the-restoration-of-wnt-signaling
#6
Zhiqi Song, Wei Yang, Xiangmei Zhou, Lifeng Yang, Deming Zhao
Prion diseases are a group of infectious neurodegenerative diseases characterized by multiple neuropathological hallmarks, including accumulation of PrP(Sc), synaptic damage, and neuronal death. We previously reported that the repressor element 1-silencing transcription factor (REST), a novel neuroprotective marker in neurodegeneration, protects neurons against neurotoxic peptide (PrP106-126)-induced neurotoxicity, but fails to maintain survival following prolonged exposure to PrP106-126. Because Wnt signaling partially induces REST and is activated by lithium, we investigated the effects of lithium on REST in prion diseases...
May 22, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28545724/the-role-of-ca-2-in-cell-death-caused-by-oxidative-glutamate-toxicity-and-ferroptosis
#7
REVIEW
Pamela Maher, Klaus van Leyen, Partha Narayan Dey, Birgit Honrath, Amalia Dolga, Axel Methner
Ca(2+) ions play a fundamental role in cell death mediated by oxidative glutamate toxicity or oxytosis, a form of programmed cell death similar and possibly identical to other forms of cell death like ferroptosis. Ca(2+) influx from the extracellular space occurs late in a cascade characterized by depletion of the intracellular antioxidant glutathione, increases in cytosolic reactive oxygen species and mitochondrial dysfunction. Here, we aim to compare oxidative glutamate toxicity with ferroptosis, address the signaling pathways that culminate in Ca(2+) influx and cell death and discuss the proteins that mediate this...
May 12, 2017: Cell Calcium
https://www.readbyqxmd.com/read/28545550/genetic-variation-in-neurodegenerative-diseases-and-its-accessibility-in-the-model-organism-caenorhabditis-elegans
#8
REVIEW
Yiru Anning Wang, Jan Edward Kammenga, Simon Crawford Harvey
BACKGROUND: Neurodegenerative diseases (NGDs) such as Alzheimer's and Parkinson's are debilitating and largely untreatable conditions strongly linked to age. The clinical, neuropathological, and genetic components of NGDs indicate that neurodegeneration is a complex trait determined by multiple genes and by the environment. MAIN BODY: The symptoms of NGDs differ among individuals due to their genetic background, and this variation affects the onset and progression of NGD and NGD-like states...
May 25, 2017: Human Genomics
https://www.readbyqxmd.com/read/28545543/inhibition-of-colony-stimulating-factor-1-receptor-early-in-disease-ameliorates-motor-deficits-in-sca1-mice
#9
Wenhui Qu, Andrea Johnson, Joo Hyun Kim, Abigail Lukowicz, Daniel Svedberg, Marija Cvetanovic
BACKGROUND: Polyglutamine (polyQ) expansion in the protein Ataxin-1 (ATXN1) causes spinocerebellar ataxia type 1 (SCA1), a fatal dominantly inherited neurodegenerative disease characterized by motor deficits, cerebellar neurodegeneration, and gliosis. Currently, there are no treatments available to delay or ameliorate SCA1. We have examined the effect of depleting microglia during the early stage of disease by using PLX, an inhibitor of colony-stimulating factor 1 receptor (CSFR1), on disease severity in a mouse model of SCA1...
May 25, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28545479/endoplasmic-reticulum-stress-and-inflammation-in-the-central-nervous-system
#10
REVIEW
Neil T Sprenkle, Savannah G Sims, Cristina L Sánchez, Gordon P Meares
Persistent endoplasmic reticulum (ER) stress is thought to drive the pathology of many chronic disorders due to its potential to elicit aberrant inflammatory signaling and facilitate cell death. In neurodegenerative diseases, the accumulation of misfolded proteins and concomitant induction of ER stress in neurons contributes to neuronal dysfunction. In addition, ER stress responses induced in the surrounding neuroglia may promote disease progression by coordinating damaging inflammatory responses, which help fuel a neurotoxic milieu...
May 25, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28545391/a-random-effects-model-for-the-identification-of-differential-splicing-reids-using-exon-and-hta-arrays
#11
Marijke Van Moerbeke, Adetayo Kasim, Willem Talloen, Joke Reumers, Hinrick W H Göhlmann, Ziv Shkedy
BACKGROUND: Alternative gene splicing is a common phenomenon in which a single gene gives rise to multiple transcript isoforms. The process is strictly guided and involves a multitude of proteins and regulatory complexes. Unfortunately, aberrant splicing events do occur which have been linked to genetic disorders, such as several types of cancer and neurodegenerative diseases (Fan et al., Theor Biol Med Model 3:19, 2006). Therefore, understanding the mechanism of alternative splicing and identifying the difference in splicing events between diseased and healthy tissue is crucial in biomedical research with the potential of applications in personalized medicine as well as in drug development...
May 25, 2017: BMC Bioinformatics
https://www.readbyqxmd.com/read/28545383/quinolinic-carboxylic-acid-derivatives-as-potential-multi-target-compounds-for-neurodegeneration-monoamine-oxidase-and-cholinesterase-inhibition
#12
Nehal Afreen Khan, Imtiaz Khan, Syed Mobasher Ali Abid, Sumera Zaib, Aliya Ibrar, Hina Andleeb, Shahid Hameed, Jamshed Iqbal
BACKGROUND: Parkinson&#039;s disease (PD), a debilitating and progressive disorder, is among the most challenging and devastating neurodegenerative diseases predominantly affecting the people over 60 years of age. OBJECTIVES: To confront PD, an advanced and operational strategy is to design single chemical functionality able to control more than one target instantaneously. METHODS: In this endeavor, for the exploration of new and efficient inhibitors of Parkinson&#039;s disease, we synthesized a series of quinoline carboxylic acids (3a‒j) and evaluated their in-vitro monoamine oxidase and cholinesterase inhibitory activities...
May 25, 2017: Medicinal Chemistry
https://www.readbyqxmd.com/read/28545363/sleep-wake-patterns-and-cognition-of-older-adults-with-amnestic-mild-cognitive-impairment-amci-a-comparison-with-cognitively-healthy-adults-and-moderate-alzheimer-s-disease-patients
#13
Emma J Wams, Gordon K Wilcock, Russell G Foster, Katharina Wulff
Age-related cognitive impairment and the prevalence of neurodegenerative disease contribute to decreasing quality of life in affected individuals and their families as well as demand considerable societal responsibility. Sleep supports overall brain activity and contributes to both physical and mental health. As a result sleep is an attractive target for exploring ways to promote health in accelerated cognitive aging. The aims of this study were to characterise cognitive performance and sleep-wake behaviour in older adults with different degrees of cognitive impairment...
May 22, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28545360/melatonin-effects-in-rem-sleep-behavior-disorder-associated-with-obstructive-sleep-apnea-syndrome-a-case-series
#14
Carolin Schaefer, Dieter Kunz, Frederik Bes
OBJECTIVES: REM sleep behavior disorder (RBD), with its main clinical symptoms of nightmares with dream-enacting behavior, is considered as a possible precursor of neurodegenerative disease. Obstructive Sleep Apnea Syndrome (OSAS) is known to be capable of provoking RBD-like symptoms by apneic event related arousals. The two sleep related pathologies must coincide in a relevant number of individuals because of overlapping prevalence in similar age groups. Until now RBD symptoms coexisting with OSAS are rarely described in scientific literature and in fact considered as OSAS mimicking RBD...
May 22, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28545157/the-aminoestrogen-prolame-increases-recognition-memory-and-hippocampal-neuronal-spine-density-in-aged-mice
#15
Alfonso Diaz, Samuel Treviño, Rubén Vázquez-Roque, Berenice Venegas, Blanca Espinosa, Gonzalo Flores, Juan Manuel Fernández-G, Luis F Montaño, Jorge Guevara
The aging brain shows biochemical and morphological changes in the dendrites of pyramidal neurons from the limbic system associated with memory loss. Prolame (N-(3-hydroxy-1,3,5 (10) -estratrien-17β-yl) -3-hydroxypropylamine) is a non-feminizing aminoestrogen with antithrombotic activity that prevents neuronal deterioration, oxidative stress and neuroinflammation. Our aim was to evaluate the effect of prolame on motor and cognitive processes, as well as its influence on the dendritic morphology of neurons at the CA1, CA3 and granule cells of the dentate gyrus (DG) regions of hippocampus (HP), and medium spiny neurons of the nucleus accumbens (NAcc) of aged mice...
May 25, 2017: Synapse
https://www.readbyqxmd.com/read/28545141/prion-pathogenesis-is-unaltered-in-the-absence-of-sirp%C3%AE-mediated-don-t-eat-me-signaling
#16
Mario Nuvolone, Marta Paolucci, Silvia Sorce, Veronika Kana, Rita Moos, Takashi Matozaki, Adriano Aguzzi
Prion diseases are neurodegenerative conditions caused by misfolding of the prion protein, leading to conspicuous neuronal loss and intense microgliosis. Recent experimental evidence point towards a protective role of microglia against prion-induced neurodegeneration, possibly through elimination of prion-containing apoptotic bodies. The molecular mechanisms by which microglia recognize and eliminate apoptotic cells in the context of prion diseases are poorly defined. Here we investigated the possible involvement of signal regulatory protein α (SIRPα), a key modulator of host cell phagocytosis; SIRPα is encoded by the Sirpa gene that is genetically linked to the prion gene Prnp...
2017: PloS One
https://www.readbyqxmd.com/read/28544479/drinking-problems-mechanisms-of-macropinosome-formation-and-maturation
#17
REVIEW
Catherine M Buckley, Jason S King
Macropinocytosis is a mechanism for the non-specific bulk uptake and internalisation of extracellular fluid. This plays specific and distinct roles in diverse cell types such as macrophages, dendritic cells and neurons, by allowing cells to sample their environment, extract extracellular nutrients and regulate plasma membrane turnover. Macropinocytosis has recently been implicated in several diseases including cancer, neurodegenerative diseases and atherosclerosis. Uptake by macropinocytosis is also exploited by several intracellular pathogens to gain entry into host cells...
May 24, 2017: FEBS Journal
https://www.readbyqxmd.com/read/28544038/supplementation-with-herbal-extracts-to-promote-behavioral-and-neuroprotective-effects-in-experimental-models-of-parkinson-s-disease-a-systematic-review
#18
REVIEW
Ianara Mendonça da Costa, José Rodolfo Lopes de Paiva Cavalcanti, Dinalva Brito de Queiroz, Eduardo Pereira de Azevedo, Amália Cinthia Meneses do Rêgo, Irami Araújo Filho, Paulo Parente, Marco Antônio Botelho, Fausto Pierdoná Guzen
Parkinson's disease (PD) consists of a neurodegenerative pathology that has received a considerable amount of attention because of its clinical manifestations. The most common treatment consists of administering the drugs levodopa and biperiden, which reduce the effectiveness of the disease and the progress of its symptoms. However, phytotherapy treatment of PD has shown great potential in retarding the loss of dopaminergic neurons and minimizing the behavioral abnormalities. The aim of this study is to systematically review the use of supplemental herbal plants with cellular protective effect and behavioral activity in in vivo and in vitro experimental models...
May 22, 2017: Phytotherapy Research: PTR
https://www.readbyqxmd.com/read/28543935/neurodegeneration-in-ataxia-telangiectasia-multiple-roles-of-atm-kinase-in-cellular-homeostasis
#19
REVIEW
Kay Rui Choy, Dianne J Watters
Ataxia-Telangiectasia (A-T) is characterized by neuronal degeneration, cancer, diabetes, immune deficiency and increased sensitivity to ionizing radiation. A-T is attributed to the deficiency of the protein kinase coded by the ATM (Ataxia-Telangiectasia Mutated) gene. ATM is a sensor of DNA Double Strand Breaks and signals to cell cycle checkpoints and the DNA repair machinery. ATM phosphorylates numerous substrates and activates many cell-signalling pathways. There has been considerable debate about whether a defective DNA damage response is causative of the neurological aspects of the disease...
May 22, 2017: Developmental Dynamics: An Official Publication of the American Association of Anatomists
https://www.readbyqxmd.com/read/28543594/the-neuroprotective-role-of-mir-124-3p-in-a-6-hydroxydopamine-induced-cell-model-of-parkinson-s-disease-via-the-regulation-of-anax5
#20
Rui-Fang Dong, Bing Zhang, Li-Wen Tai, Hong-Mei Liu, Fang-Kun Shi, Ning-Ning Liu
Parkinson's disease (PD), the second most common neurodegenerative disorder, is characterized by a progressive loss of dopaminergic neurons in the midbrain. Several pathogenetic factors have been involved in the onset and progression of PD, including inflammation, oxidative stress, unfolded protein accumulation, and apoptosis. Ample evidence indicates that miRNAs could regulate post-transcriptional gene expression and neuronal disease. In this study, we evaluated the effects and mechanism of miR-124-3p on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in PC12 cells and SH-SY5Y cells...
May 25, 2017: Journal of Cellular Biochemistry
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