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Journal Article
PLoS ONE, ISSN 1932-6203, 02/2010, Volume 5, Issue 2, pp. e9313 - e9313
Background: Lewy body disease is a heterogeneous group of neurodegenerative disorders characterized by alpha-synuclein accumulation that includes dementia with... 
WILD-TYPE | CHAPERONE-MEDIATED AUTOPHAGY | ALZHEIMERS-DISEASE | MOUSE MODEL | FRONTOTEMPORAL DEMENTIA | BIOLOGY | AGGREGATE-PRONE PROTEINS | NEURONAL EXPRESSION | PARKINSONS-DISEASE | TRANSGENIC MICE | GAUCHER-DISEASE | Pyramidal Cells - metabolism | Humans | Nerve Degeneration - genetics | Male | Autophagy | Nerve Degeneration - metabolism | Alzheimer Disease - pathology | Brain - metabolism | Lewy Body Disease - genetics | RNA Interference | Brain - ultrastructure | Aged, 80 and over | Female | alpha-Synuclein - genetics | Pyramidal Cells - ultrastructure | Disease Models, Animal | Cell Line | Ubiquitin-Activating Enzymes - genetics | Signal Transduction | Lewy Body Disease - pathology | Mice, Transgenic | Microscopy, Electron | Ubiquitin-Activating Enzymes - metabolism | Blotting, Western | Nerve Degeneration - pathology | Lewy Body Disease - metabolism | Microscopy, Confocal | Autophagy-Related Protein 7 | Animals | Alzheimer Disease - metabolism | Brain - pathology | Cell Line, Tumor | Pyramidal Cells - pathology | Aged | Mice | Alzheimer Disease - genetics | alpha-Synuclein - metabolism | TOR protein | Neurosciences | Animal models | Parkinson's disease | Pathogenesis | Toxicity | Parkinsons disease | Phagosomes | Nervous system | Synuclein | Neuromodulation | Accumulation | Modulators | Proteins | Infusion | Alterations | Neurodegeneration | Dementia disorders | Alzheimer's disease | Movement disorders | Enzymes | Neurodegenerative diseases | Neurons | Immunomodulation | Lewy body disease | Transgenic mice | Rapamycin | Patients | Lewy bodies | Studies | Pathology | Mutation | Alzheimers disease | Phagocytosis | Apoptosis | Dementia | Index Medicus
Journal Article
Journal Article
Human Molecular Genetics, ISSN 0964-6906, 2014, Volume 23, Issue 15, pp. 3943 - 3957
Gaucher disease, a prevalent lysosomal storage disease (LSD), is caused by insufficient activity of acid beta-glucosidase (GCase) and the resultant... 
CYTOCHROME-C-OXIDASE | CONDURITOL-B-EPOXIDE | LEWY BODY DISORDERS | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE MODEL | GENETICS & HEREDITY | A-BETA | ACID-BETA-GLUCOSIDASE | AMYLOID PRECURSOR PROTEIN | ALPHA-SYNUCLEIN | PARKINSONS-DISEASE | Neurons - pathology | Microtubule-Associated Proteins - genetics | Substantia Nigra - pathology | Microtubule-Associated Proteins - metabolism | Humans | Cerebral Cortex - pathology | Mitochondrial Proteins - genetics | Gaucher Disease - pathology | Substantia Nigra - metabolism | Corpus Striatum - metabolism | Cerebral Cortex - metabolism | beta-Glucosidase - antagonists & inhibitors | Membrane Transport Proteins - genetics | Mitochondrial Proteins - metabolism | beta-Glucosidase - genetics | Amyloid beta-Protein Precursor - metabolism | beta-Glucosidase - metabolism | Membrane Transport Proteins - metabolism | Neurons - metabolism | alpha-Synuclein - genetics | Corpus Striatum - pathology | Disease Models, Animal | Prostaglandin-Endoperoxide Synthases - genetics | Inositol - pharmacology | Lysosome-Associated Membrane Glycoproteins - metabolism | Gaucher Disease - metabolism | Cells, Cultured | Enzyme Inhibitors - pharmacology | Gene Expression Regulation | Hippocampus - pathology | Mitochondria - metabolism | Mitochondria - pathology | Inositol - analogs & derivatives | Protein Aggregation, Pathological | Hippocampus - metabolism | Amyloid beta-Protein Precursor - genetics | Animals | Gaucher Disease - genetics | Prostaglandin-Endoperoxide Synthases - metabolism | Lysosome-Associated Membrane Glycoproteins - genetics | Mice | alpha-Synuclein - metabolism | Index Medicus
Journal Article
Journal Article
Journal Article
Movement Disorders, ISSN 0885-3185, 10/2017, Volume 32, Issue 10, pp. 1409 - 1422
Background: Heterozygous mutations in the GBA1 gene, which encodes the lysosomal enzyme beta-glucocerebrosidase-1, increase the risk of developing Parkinson's... 
multilamellar bodies | ER stress | cell death | autophagic vesicles | mitochondria | CANCER-CELLS | BETA-GLUCOCEREBROSIDASE | ENDOCYTIC PATHWAY | ALPHA-SYNUCLEIN | AUTOPHAGIC VACUOLES | FIBROBLASTS | CLINICAL NEUROLOGY | GAUCHER-DISEASE | ENDOPLASMIC-RETICULUM | DYSFUNCTION | GLUCOCEREBROSIDASE ACTIVITY | Glucosylceramidase - genetics | TOR Serine-Threonine Kinases - metabolism | Humans | Endoplasmic Reticulum - metabolism | Male | Fibroblasts - ultrastructure | Endoplasmic Reticulum - ultrastructure | Lysosomes - metabolism | Female | Parkinson Disease - metabolism | Autophagy - genetics | Calnexin - metabolism | Golgi Apparatus - ultrastructure | Asparagine - genetics | Parkinson Disease - pathology | Oxidative Stress - genetics | Serine - genetics | Parkinson Disease - genetics | Cholesterol - metabolism | Fibroblasts - pathology | Mutation - genetics | Lysosomes - ultrastructure | Models, Biological | Golgi Apparatus - metabolism | Lysosomal-Associated Membrane Protein 1 - metabolism | Beclin-1 - metabolism | Transcription Factor CHOP - metabolism | Calnexin - ultrastructure | Enzymes | Genetic aspects | Analysis | Cholesterol | Flow cytometry | Reactive oxygen species | Parkinson's disease | Parkinsons disease | Homeostasis | Lysosomes | mRNA | Autophagy | Mitochondria | Protein folding | Fibroblasts | Membrane potential | Protein transport | Movement disorders | Oxygen | Neurodegenerative diseases | Electron microscopy | Golgi apparatus | Storage diseases | Cell death | Glucosylceramidase | Mutation | Immunofluorescence | Endoplasmic reticulum | Phagocytosis | Apoptosis | Index Medicus
Journal Article