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Nature, ISSN 0028-0836, 05/2017, Volume 545, Issue 7652, pp. 108 - 111
Nine neurodegenerative diseases are caused by expanded polyglutamine (polyQ) tracts in different proteins, such as huntingtin in Huntington's disease and... 
PATHOGENESIS | CELLS | PROTEIN | MULTIDISCIPLINARY SCIENCES | MACHADO-JOSEPH-DISEASE | MUTANT HUNTINGTIN | ATAXIN-3 | INTRANUCLEAR INCLUSIONS | LC3 | MOUSE MODELS | AGGREGATION | Humans | Ubiquitin - metabolism | Male | Neurons - cytology | Autophagy | Brain - metabolism | Peptides - metabolism | Protein Domains | Ataxin-3 - chemistry | Female | Food Deprivation | Neurons - metabolism | Protein Stability | Ataxin-3 - metabolism | Disease Models, Animal | Binding, Competitive | Cell Line | Ataxin-3 - deficiency | Huntingtin Protein - metabolism | Mice, Inbred C57BL | Phagosomes - metabolism | Cells, Cultured | Mutant Proteins - genetics | Exons - genetics | Mutant Proteins - metabolism | Huntington Disease - metabolism | Huntingtin Protein - chemistry | Animals | Mutant Proteins - chemistry | Brain - pathology | Huntington Disease - genetics | Protein Binding | Mice | Huntingtin Protein - genetics | Mutation | Proteasome Endopeptidase Complex - metabolism | Beclin-1 - metabolism | Ataxin-3 - genetics | Physiological aspects | Autophagy (Cytology) | Neural circuitry | Observations | Huntingtons disease | Competition | Biotechnology | Huntingtin | Toxicity | Pathogenesis | Impairment | Biosynthesis | Kinases | Experiments | Degradation | Proteins | Scholarships & fellowships | Ataxin | Rodents | Spinocerebellar ataxia | Ataxia | Biocompatibility | Trinucleotide repeat diseases | Medical research | Starvation | Neurodegenerative diseases | Polyglutamine diseases | Huntington's disease | Neurological diseases | Machado-Joseph disease | Cell lines | Scientific imaging | Mass spectrometry | Phagocytosis | Index Medicus
Journal Article
Annual Review of Neuroscience, ISSN 0147-006X, 2007, Volume 30, Issue 1, pp. 575 - 621
The discovery that expansion of unstable repeats can cause a variety of neurological disorders has changed the landscape of disease-oriented research for... 
Unstable repeats | Polyglutamine | Ataxin | Frataxin | Myotonic dystrophy | Huntington disease | Ataxia | Fragile X syndrome | Mental retardation | Spinal bulbar muscular atrophy | SPINOCEREBELLAR ATAXIA TYPE-1 | UBIQUITIN-PROTEASOME SYSTEM | unstable repeats | fragile X syndrome | polyglutamine | NEUROSCIENCES | X MENTAL-RETARDATION | frataxin | myotonic dystrophy | mental retardation | HUNTINGTONS-DISEASE GENE | ataxia | spinal bulbar muscular atrophy | MACHADO-JOSEPH-DISEASE | ataxin | TRANSGENIC MOUSE MODEL | DENTATORUBRAL-PALLIDOLUYSIAN ATROPHY | DOMINANT CEREBELLAR-ATAXIA | BULBAR MUSCULAR-ATROPHY | FMR1 KNOCKOUT MICE | Fragile X Syndrome - genetics | Heredodegenerative Disorders, Nervous System - genetics | Genetic Predisposition to Disease - genetics | Cerebellar Ataxia - metabolism | Brain - physiopathology | Fragile X Syndrome - physiopathology | Humans | Peptides - genetics | Fragile X Syndrome - metabolism | Heredodegenerative Disorders, Nervous System - physiopathology | Mutation - genetics | Huntington Disease - metabolism | Brain - metabolism | Cerebellar Ataxia - physiopathology | Animals | Cerebellar Ataxia - genetics | Peptides - metabolism | Huntington Disease - genetics | Trinucleotide Repeat Expansion - genetics | Heredodegenerative Disorders, Nervous System - metabolism | Huntington Disease - physiopathology | Trinucleotide repeats | Care and treatment | Genetic aspects | Diagnosis
Journal Article
Neuron, ISSN 0896-6273, 03/2017, Volume 93, Issue 5, pp. 1015 - 1034
Autophagy is a conserved pathway that delivers cytoplasmic contents to the lysosome for degradation. Here we consider its roles in neuronal health and disease.... 
motor neuron disease | autophagy | Alzheimer’s disease | neurodegeneration | dementia | tau | Huntington’s disease | lysosome | Parkinson’s disease | Parkinson's disease | Huntington's disease | Alzheimer's disease | NEURAL STEM-CELLS | PARKIN-DEFICIENT MICE | HEREDITARY SPASTIC PARAPARESIS | MACHADO-JOSEPH-DISEASE | TAUOPATHY IN-VITRO | AGGREGATE-PRONE PROTEINS | NUCLEOTIDE EXCHANGE FACTOR | AMYOTROPHIC-LATERAL-SCLEROSIS | LYSOSOMAL STORAGE DISORDERS | TRANSGENIC MOUSE MODEL | NEUROSCIENCES | Animals | Lysosomes - metabolism | Neurodegenerative Diseases - pathology | Proteins - metabolism | Humans | Neurodegenerative Diseases - therapy | Signal Transduction - physiology | Autophagy - physiology | Neurodegenerative Diseases - metabolism | Motor Neurons - pathology | Nervous system diseases | Cell differentiation | Health aspects | Stem cells | Medical genetics | Medical research | Neurons | Medicine, Experimental | Drug discovery | Brain | Cargo | Phosphorylation | Regulators | Energy levels | Amino acid starvation | Homeostasis | Amino acids | Chains | Homology | AKT protein | Activation | Kinases | Autophagy | Neurogenesis | Lipid bilayers | Defects | Proteins | Allosteric properties | Neurodegeneration | Rodents | Nutrients | Aspartic acid | Degeneration | Growth factors | Assembly | Elongation | Enzymes | Pathogens | Berberine | Starvation | AMP | BRCA1 protein | Amyotrophic lateral sclerosis | Longevity | Sun | Survival | Adhesion | 1-Phosphatidylinositol 3-kinase | Peroxisomes | Phototransduction | Aggregates | Protein kinase | Cell death | β-Amyloid | Aberration | Apoptosis
Journal Article
Molecular Therapy, ISSN 1525-0016, 10/2013, Volume 21, Issue 10, pp. 1898 - 1908
Journal Article