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post mortem brain autophage

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https://www.readbyqxmd.com/read/26936765/autophagic-and-lysosomal-defects-in-human-tauopathies-analysis-of-post-mortem-brain-from-patients-with-familial-alzheimer-disease-corticobasal-degeneration-and-progressive-supranuclear-palsy
#1
Antonio Piras, Ludovic Collin, Fiona Grüninger, Caroline Graff, Annica Rönnbäck
INTRODUCTION: The accumulation of insoluble proteins within neurons and glia cells is a pathological hallmark of several neurodegenerative diseases. Abnormal aggregation of the microtubule-associated protein tau characterizes the neuropathology of tauopathies, such as Alzheimer disease (AD), corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP). An impairment of the lysosomal degradation pathway called macroautophagy, hereafter referred to as autophagy, could contribute to the accumulation of aggregated proteins...
March 2, 2016: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/26930584/evidence-for-the-recruitment-of-autophagic-vesicles-in-human-brain-after-stroke
#2
Tony Frugier, Juliet M Taylor, Catriona McLean, Nicole Bye, Philip M Beart, Rodney J Devenish, Peter J Crack
Autophagy is a homeostatic process for recycling proteins and organelles that is increasingly being proposed as a therapeutic target for acute and chronic neurodegenerative diseases, including stroke. Confirmation that autophagy is present in the human brain after stroke is imperative before prospective therapies can begin the translational process into clinical trials. Our current study using human post-mortem tissue observed an increase in staining in microtubule-associated protein 1 light chain 3 (LC3), sequestosome 1 (SQSTM1; also known as p62) and the increased appearance of autophagic vesicles after stroke...
June 2016: Neurochemistry International
https://www.readbyqxmd.com/read/26302676/serine-403-phosphorylated-p62-sqstm1-immunoreactivity-in-inclusions-of-neurodegenerative-diseases
#3
Masaru Kurosawa, Gen Matsumoto, Hiroyuki Sumikura, Hiroyuki Hatsuta, Shigeo Murayama, Takashi Sakurai, Tomomi Shimogori, Nobutaka Hattori, Nobuyuki Nukina
Protein inclusions in neurodegenerative diseases are associated with p62, which has an important role in autophagic clearance of polyubiquitinated proteins. Selective autophagy is regulated by S403-phosphorylation of p62, and S403-phosphorylated p62 (S403-phos-p62) accumulates in Atg5 conditional knockout (Atg5CKO) mice in which autophagosome formation is impaired. We performed immunohistochemical tests for the presence of S403-phos-p62 in postmortem brain of neurodegenerative disease cases, and found accumulations in amyotrophic lateral sclerosis and Alzheimer's disease tissues...
February 2016: Neuroscience Research
https://www.readbyqxmd.com/read/26217309/differing-roles-of-autophagy-in-hiv-associated-neurocognitive-impairment-and-encephalitis-with-implications-for-morphine-co-exposure
#4
Seth M Dever, Myosotys Rodriguez, Jessica Lapierre, Blair N Costin, Nazira El-Hage
We investigated the role of autophagy in HIV-infected subjects with neurocognitive impairment (NCI) ± HIV encephalitis (HIVE), many of which had a history of polysubstance abuse/dependence, using post-mortem brain tissues to determine whether differences in autophagy related factors may be more associated with NCI or NCI-encephalitis. Using qRT-PCR, we detected significant differences in gene expression levels with SQSTM1, LAMP1 higher in HIV-infected subjects without NCI while ATG5, SQSTM1 were then lower in HIV infection/NCI and ATG7, SQSTM1 being higher in NCI-HIVE...
2015: Frontiers in Microbiology
https://www.readbyqxmd.com/read/25791428/mtor-mediates-tau-localization-and-secretion-implication-for-alzheimer-s-disease
#5
Zhi Tang, Eniko Ioja, Erika Bereczki, Kjell Hultenby, Chunxia Li, Zhizhong Guan, Bengt Winblad, Jin-Jing Pei
Abnormally hyperphosphorylated tau aggregates form paired helical filaments (PHFs) in neurofibrillary tangles, a key hallmark of Alzheimer's disease (AD) and other tauopathies. The cerebrospinal fluid (CSF) levels of soluble total tau and phospho-tau from clinically diagnosed AD patients are significantly higher compared with controls. Data from both in vitro and in vivo AD models have implied that an aberrant increase of mammalian target of rapamycin (mTor) signaling may be a causative factor for the formation of abnormally hyperphosphorylated tau...
July 2015: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/24477431/reduced-glucocerebrosidase-is-associated-with-increased-%C3%AE-synuclein-in-sporadic-parkinson-s-disease
#6
Karen E Murphy, Amanda M Gysbers, Sarah K Abbott, Nahid Tayebi, Woojin S Kim, Ellen Sidransky, Antony Cooper, Brett Garner, Glenda M Halliday
Heterozygous mutations in GBA1, the gene encoding lysosomal glucocerebrosidase, are the most frequent known genetic risk factor for Parkinson's disease. Reduced glucocerebrosidase and α-synuclein accumulation are directly related in cell models of Parkinson's disease. We investigated relationships between Parkinson's disease-specific glucocerebrosidase deficits, glucocerebrosidase-related pathways, and α-synuclein levels in brain tissue from subjects with sporadic Parkinson's disease without GBA1 mutations...
March 2014: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/24444419/tnfaip8%C3%A2-l1-oxi-%C3%AE-binds-to-fbxw5-increasing-autophagy-through-activation-of-tsc2-in-a-parkinson-s-disease-model
#7
Ji-Young Ha, Ji-Soo Kim, Young-Hee Kang, Eugene Bok, Yoon-Seong Kim, Jin H Son
Abnormal autophagy may contribute to neurodegeneration in Parkinson's disease (PD). However, it is largely unknown how autophagy is dysregulated by oxidative stress (OS), one of major pathogenic causes of PD. We recently discovered the potential autophagy regulator gene family including Tnfaip8/Oxi-α, which is a mammalian target of rapamycin (mTOR) activator down-regulated by OS in dopaminergic neurons (J. Neurochem., 112, 2010, 366). Here, we demonstrate that the OS-induced Tnfaip8 l1/Oxi-β could increase autophagy by a unique mechanism that increases the stability of tuberous sclerosis complex 2 (TSC2), a critical negative regulator of mTOR...
May 2014: Journal of Neurochemistry
https://www.readbyqxmd.com/read/22291444/disrupted-in-schizophrenia-1-forms-pathological-aggresomes-that-disrupt-its-function-in-intracellular-transport
#8
Talia A Atkin, Nicholas J Brandon, Josef T Kittler
Disrupted in Schizophrenia 1 (DISC1) is a key susceptibility gene implicated in major mental illnesses, such as schizophrenia, depression, bipolar disorder and autism, but the link between this protein and the pathology of these diseases remains unclear. Recently, DISC1 has been demonstrated to form insoluble protein aggregates in vitro and in human post-mortem brain tissue but the cellular dynamics of these DISC1 aggregates and their effects on neuronal function are unknown. Using a combination of biochemistry and live cell confocal and video microscopy, we characterize the properties of DISC1 aggregates and their effects on cellular function...
May 1, 2012: Human Molecular Genetics
https://www.readbyqxmd.com/read/20946470/granulovacuolar-degeneration-gvd-bodies-of-alzheimer-s-disease-ad-resemble-late-stage-autophagic-organelles
#9
K E Funk, R E Mrak, J Kuret
AIMS: Granulovacuolar degeneration involves the accumulation of large, double membrane-bound bodies within certain neurones during the course of Alzheimer's disease (AD) and other adult-onset dementias. Because of the two-layer membrane morphology, it has been proposed that the bodies are related to autophagic organelles. The aim of this study was to test this hypothesis, and determine the approximate stage at which the pathway stalls in AD. METHODS: Spatial colocalization of autophagic and endocytic markers with casein kinase 1 delta, a marker for granulovacuolar degeneration (GVD) bodies, was evaluated in hippocampal sections prepared from post mortem Braak stage IV and V AD cases using double-label confocal fluorescence microscopy...
April 2011: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/19075733/ischemic-neuronal-damage
#10
REVIEW
Era Taoufik, Lesley Probert
Knowledge of the molecular mechanisms that underlie neuron death following stroke is important to allow the development of effective neuroprotective strategies. Since studies in human stroke are extremely limited due to the inability of collecting post mortem tissue at time points after the onset of stroke where neuronal death occurs, brain ischemia research focuses on information derived from animal models of ischemic injury. The two principal models for human stroke are induced in rodents either by global or focal ischemia...
2008: Current Pharmaceutical Design
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