Nature Genetics, ISSN 1061-4036, 2012, Volume 44, Issue 5, pp. 552 - 561
Identifying genetic variants influencing human brain structures may reveal new biological mechanisms underlying cognition and neuropsychiatric illness. The...
AUTOMATED SEGMENTATION | HUMAN HEIGHT | FUNCTIONAL IMPLICATIONS | TEMPORAL-LOBE EPILEPSY | UNIFIED APPROACH | GENOTYPE IMPUTATION | ALZHEIMERS-DISEASE | GENETICS & HEREDITY | BRAIN VOLUME | NA+/H+ EXCHANGER | GENOME-WIDE ASSOCIATION | Neuroimaging | Genome-Wide Association Study | Meta-Analysis as Topic | Brain - physiopathology | Humans | Polymorphism, Single Nucleotide - genetics | Genetic Loci | Genetic Markers | Chromosomes, Human, Pair 12 - genetics | Hippocampus - physiopathology | Head | Genetic aspects | Hippocampus (Brain) | Genetic variation | Identification and classification | Body size | Studies | Haplotypes | Neurology | Brain | Genealogy | Statistical analysis | Quality control | Genetics | Genomes | Meta-analysis | Life Sciences | Neurons and Cognition
AUTOMATED SEGMENTATION | HUMAN HEIGHT | FUNCTIONAL IMPLICATIONS | TEMPORAL-LOBE EPILEPSY | UNIFIED APPROACH | GENOTYPE IMPUTATION | ALZHEIMERS-DISEASE | GENETICS & HEREDITY | BRAIN VOLUME | NA+/H+ EXCHANGER | GENOME-WIDE ASSOCIATION | Neuroimaging | Genome-Wide Association Study | Meta-Analysis as Topic | Brain - physiopathology | Humans | Polymorphism, Single Nucleotide - genetics | Genetic Loci | Genetic Markers | Chromosomes, Human, Pair 12 - genetics | Hippocampus - physiopathology | Head | Genetic aspects | Hippocampus (Brain) | Genetic variation | Identification and classification | Body size | Studies | Haplotypes | Neurology | Brain | Genealogy | Statistical analysis | Quality control | Genetics | Genomes | Meta-analysis | Life Sciences | Neurons and Cognition
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The ENIGMA Consortium: large-scale collaborative analyses of neuroimaging and genetic data
Brain imaging and behavior, ISSN 1931-7557, 2014, Volume 8, Issue 2, pp. 153 - 182
The Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Consortium is a collaborative network of researchers working together on a range of...
Neurosciences | Biomedicine | GWAS | MRI | Multi-site | Consortium | Genetics | Neuropsychology | Psychiatry | Neuroradiology | Meta-analysis | COMMON VARIANTS | ALZHEIMERS-DISEASE | HIPPOCAMPAL ATROPHY | NEUROIMAGING | APOLIPOPROTEIN-E | QUANTITATIVE TRAIT LOCI | HUMAN BRAIN STRUCTURE | CORTICAL SURFACE-AREA | MULTIVARIATE PARALLEL ICA | WHITE-MATTER MICROSTRUCTURE | GENOME-WIDE ASSOCIATION | Neuroimaging - methods | Cooperative Behavior | Meta-Analysis as Topic | Brain Mapping - methods | Genome-Wide Association Study - methods | Humans | Medicine | Consortia | Neuroimaging | Usage | Conferences, meetings and seminars | Analysis | Life Sciences | Neurons and Cognition | Genetic Neuroimaging in Aging and Age-Related Diseases | Basic Medicine | Social Sciences | Medical and Health Sciences | Medicin och hälsovetenskap | Psychology | Samhällsvetenskap | Medicinska och farmaceutiska grundvetenskaper | Psykologi | Neurovetenskaper
Neurosciences | Biomedicine | GWAS | MRI | Multi-site | Consortium | Genetics | Neuropsychology | Psychiatry | Neuroradiology | Meta-analysis | COMMON VARIANTS | ALZHEIMERS-DISEASE | HIPPOCAMPAL ATROPHY | NEUROIMAGING | APOLIPOPROTEIN-E | QUANTITATIVE TRAIT LOCI | HUMAN BRAIN STRUCTURE | CORTICAL SURFACE-AREA | MULTIVARIATE PARALLEL ICA | WHITE-MATTER MICROSTRUCTURE | GENOME-WIDE ASSOCIATION | Neuroimaging - methods | Cooperative Behavior | Meta-Analysis as Topic | Brain Mapping - methods | Genome-Wide Association Study - methods | Humans | Medicine | Consortia | Neuroimaging | Usage | Conferences, meetings and seminars | Analysis | Life Sciences | Neurons and Cognition | Genetic Neuroimaging in Aging and Age-Related Diseases | Basic Medicine | Social Sciences | Medical and Health Sciences | Medicin och hälsovetenskap | Psychology | Samhällsvetenskap | Medicinska och farmaceutiska grundvetenskaper | Psykologi | Neurovetenskaper
Journal Article
Frontiers in Neuroscience, ISSN 1662-453X, 03/2019, Volume 13
Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of...
Vector-borne diseases | Animal models | Parkinson's disease | Disease | Neurodegenerative diseases | Pathogenesis | Genes | Cytotoxicity | Amyotrophic lateral sclerosis | Genomes | Lymphocytes T | Ribonucleic acid--RNA | Gene expression | Gingivitis | Microglia | Neurotoxicity | Neurodegeneration | Autopsy | Aging | Tumor necrosis factor-TNF | Alzheimer's disease | Movement disorders | neurodegeneration | ALS | Alzheimer’s disease | microglia | Parkinson’s disease | gene expression
Vector-borne diseases | Animal models | Parkinson's disease | Disease | Neurodegenerative diseases | Pathogenesis | Genes | Cytotoxicity | Amyotrophic lateral sclerosis | Genomes | Lymphocytes T | Ribonucleic acid--RNA | Gene expression | Gingivitis | Microglia | Neurotoxicity | Neurodegeneration | Autopsy | Aging | Tumor necrosis factor-TNF | Alzheimer's disease | Movement disorders | neurodegeneration | ALS | Alzheimer’s disease | microglia | Parkinson’s disease | gene expression
Journal Article
FRONTIERS IN NEUROSCIENCE, ISSN 1662-453X, 03/2019, Volume 13, p. 235
Nervous tissues from both humans with neurodegenerative diseases (NDD) and animals with genetic models of human NDD, such as rare monogenic causes of...
CELLS | Parkinson's disease | neurodegeneration | ALS | MECHANISMS | NEUROSCIENCES | MOLECULES | NEUROINFLAMMATION | PATHWAY | ROLES | HEALTH | STRESS | microglia | Alzheimer's disease | gene expression | PROGRESSION | RNA sequencing | Amyotrophic lateral sclerosis | RNA | T cells | Genes
CELLS | Parkinson's disease | neurodegeneration | ALS | MECHANISMS | NEUROSCIENCES | MOLECULES | NEUROINFLAMMATION | PATHWAY | ROLES | HEALTH | STRESS | microglia | Alzheimer's disease | gene expression | PROGRESSION | RNA sequencing | Amyotrophic lateral sclerosis | RNA | T cells | Genes
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2016, Volume 11, Issue 8, p. e0160520
ALS is a rapidly progressive, devastating neurodegenerative illness of adults that produces disabling weakness and spasticity arising from death of lower and...
Inflammation - pathology | Genome-Wide Association Study | Spinal Cord - metabolism | Amyotrophic Lateral Sclerosis - genetics | Humans | Tumor Necrosis Factor-alpha - genetics | Signal Transduction - genetics | Gene Regulatory Networks | Case-Control Studies | Motor Neurons - pathology | Amyotrophic Lateral Sclerosis - complications | Motor Neurons - metabolism | Spinal Cord - immunology | Amyotrophic Lateral Sclerosis - pathology | Sequence Analysis, RNA | Autopsy | Spinal Cord - pathology | Tumor Necrosis Factor-alpha - physiology | Inflammation - genetics | High-Throughput Nucleotide Sequencing | RNA sequencing | RNA | Neurons | Genes | Genomics | Development and progression | Genomes | Inflammation | DNA binding proteins | Genetic transcription | Necrosis | Algorithms | Tumor necrosis factor | Cell death | Analysis | Tumors | Spinal cord | Transcription factors | Pathogenesis | Cytotoxicity | Lymphocytes T | Retinoid X receptor α | Activation | Macrophages | Caspase-3 | Gene sequencing | Proteins | Network analysis | Tumor necrosis factor-TNF | Physiology | Bioinformatics | Motor neurons | NF-κB protein | rRNA | Abnormalities | Spasticity | Caspase | Amyotrophic lateral sclerosis | Biophysics | Tumor necrosis factor-α | Gene expression | Ribonucleic acid--RNA | Studies | Pathology | Signaling | Adults | Mutation | Molecular biology | Viability | Chemokines | Ribonucleic acid
Inflammation - pathology | Genome-Wide Association Study | Spinal Cord - metabolism | Amyotrophic Lateral Sclerosis - genetics | Humans | Tumor Necrosis Factor-alpha - genetics | Signal Transduction - genetics | Gene Regulatory Networks | Case-Control Studies | Motor Neurons - pathology | Amyotrophic Lateral Sclerosis - complications | Motor Neurons - metabolism | Spinal Cord - immunology | Amyotrophic Lateral Sclerosis - pathology | Sequence Analysis, RNA | Autopsy | Spinal Cord - pathology | Tumor Necrosis Factor-alpha - physiology | Inflammation - genetics | High-Throughput Nucleotide Sequencing | RNA sequencing | RNA | Neurons | Genes | Genomics | Development and progression | Genomes | Inflammation | DNA binding proteins | Genetic transcription | Necrosis | Algorithms | Tumor necrosis factor | Cell death | Analysis | Tumors | Spinal cord | Transcription factors | Pathogenesis | Cytotoxicity | Lymphocytes T | Retinoid X receptor α | Activation | Macrophages | Caspase-3 | Gene sequencing | Proteins | Network analysis | Tumor necrosis factor-TNF | Physiology | Bioinformatics | Motor neurons | NF-κB protein | rRNA | Abnormalities | Spasticity | Caspase | Amyotrophic lateral sclerosis | Biophysics | Tumor necrosis factor-α | Gene expression | Ribonucleic acid--RNA | Studies | Pathology | Signaling | Adults | Mutation | Molecular biology | Viability | Chemokines | Ribonucleic acid
Journal Article
Biochemical Pharmacology, ISSN 0006-2952, 10/2016, Volume 117, pp. 68 - 77
Microneurotrophins (MNT’s) are small molecule derivatives of dehydroepiandrosterone (DHEA) and do not have significant interactions with sex steroid receptors....
RNA-sequencing | Gene ontology | ALS | Microneurotrophin | iPSC-derived motor neuron | MOTOR-NEURONS | STEM-CELLS | NEUROSTEROIDS | DEHYDROEPIANDROSTERONE | P-GLYCOPROTEIN | STRATEGIES | ALIGNMENT | PHARMACOLOGY & PHARMACY | GENERATION | RECEPTORS | CANCER RESISTANCE PROTEIN | Drugs, Investigational - pharmacology | Humans | Drugs, Investigational - pharmacokinetics | Hepatocytes - pathology | Drugs, Investigational - metabolism | Hepatocytes - metabolism | Neural Stem Cells - cytology | Dehydroepiandrosterone - analogs & derivatives | Amyotrophic Lateral Sclerosis - drug therapy | Motor Neurons - pathology | Neuroprotective Agents - metabolism | Tissue Distribution | Hepatocytes - cytology | Neuroprotective Agents - pharmacology | Neuroprotective Agents - pharmacokinetics | Biotransformation | Dehydroepiandrosterone - pharmacokinetics | Membrane Transport Modulators - pharmacology | Motor Neurons - cytology | Madin Darby Canine Kidney Cells | Dehydroepiandrosterone - metabolism | Induced Pluripotent Stem Cells - cytology | ATP Binding Cassette Transporter, Sub-Family B - antagonists & inhibitors | Hepatocytes - drug effects | Motor Neurons - drug effects | Caco-2 Cells | Recombinant Proteins - metabolism | Absorption, Physiological - drug effects | Cell Line | Induced Pluripotent Stem Cells - drug effects | Dehydroepiandrosterone - pharmacology | Cells, Cultured | Neural Stem Cells - drug effects | Recombinant Proteins - chemistry | Nerve Tissue Proteins - genetics | Gene Expression Regulation - drug effects | Motor Neurons - metabolism | Nerve Tissue Proteins - metabolism | Amyotrophic Lateral Sclerosis - pathology | Animals | Amyotrophic Lateral Sclerosis - metabolism | Dogs | ATP Binding Cassette Transporter, Sub-Family B - metabolism | Mice | ATP Binding Cassette Transporter, Sub-Family B - genetics | Blood-Brain Barrier | Amyotrophic lateral sclerosis | Drug therapy | Real estate development | Analysis
RNA-sequencing | Gene ontology | ALS | Microneurotrophin | iPSC-derived motor neuron | MOTOR-NEURONS | STEM-CELLS | NEUROSTEROIDS | DEHYDROEPIANDROSTERONE | P-GLYCOPROTEIN | STRATEGIES | ALIGNMENT | PHARMACOLOGY & PHARMACY | GENERATION | RECEPTORS | CANCER RESISTANCE PROTEIN | Drugs, Investigational - pharmacology | Humans | Drugs, Investigational - pharmacokinetics | Hepatocytes - pathology | Drugs, Investigational - metabolism | Hepatocytes - metabolism | Neural Stem Cells - cytology | Dehydroepiandrosterone - analogs & derivatives | Amyotrophic Lateral Sclerosis - drug therapy | Motor Neurons - pathology | Neuroprotective Agents - metabolism | Tissue Distribution | Hepatocytes - cytology | Neuroprotective Agents - pharmacology | Neuroprotective Agents - pharmacokinetics | Biotransformation | Dehydroepiandrosterone - pharmacokinetics | Membrane Transport Modulators - pharmacology | Motor Neurons - cytology | Madin Darby Canine Kidney Cells | Dehydroepiandrosterone - metabolism | Induced Pluripotent Stem Cells - cytology | ATP Binding Cassette Transporter, Sub-Family B - antagonists & inhibitors | Hepatocytes - drug effects | Motor Neurons - drug effects | Caco-2 Cells | Recombinant Proteins - metabolism | Absorption, Physiological - drug effects | Cell Line | Induced Pluripotent Stem Cells - drug effects | Dehydroepiandrosterone - pharmacology | Cells, Cultured | Neural Stem Cells - drug effects | Recombinant Proteins - chemistry | Nerve Tissue Proteins - genetics | Gene Expression Regulation - drug effects | Motor Neurons - metabolism | Nerve Tissue Proteins - metabolism | Amyotrophic Lateral Sclerosis - pathology | Animals | Amyotrophic Lateral Sclerosis - metabolism | Dogs | ATP Binding Cassette Transporter, Sub-Family B - metabolism | Mice | ATP Binding Cassette Transporter, Sub-Family B - genetics | Blood-Brain Barrier | Amyotrophic lateral sclerosis | Drug therapy | Real estate development | Analysis
Journal Article
Schizophrenia Bulletin, ISSN 0586-7614, 03/2013, Volume 39, Issue 2, pp. 330 - 338
Low serum folate levels previously have been associated with negative symptom risk in schizophrenia, as has the hypofunctional 677C>T variant of the MTHFR...
genetic risk score | methylation | epigenetics | gene-environment interaction | BLADDER-CANCER | DEPRESSION | PSYCHIATRY | COMMON MUTATION | DNA-METHYLATION | METHYLENETETRAHYDROFOLATE REDUCTASE | HOMOCYSTEINE LEVELS | CATECHOL-O-METHYLTRANSFERASE | POLYMORPHISMS | RISK-FACTOR | ONE-CARBON METABOLISM | Severity of Illness Index | Genetic Predisposition to Disease | Schizophrenia - metabolism | Gene Frequency | Humans | Reduced Folate Carrier Protein - genetics | Linear Models | Male | Mutation, Missense | Catechol O-Methyltransferase - genetics | Schizophrenic Psychology | Metabolic Networks and Pathways - genetics | Glutamate Carboxypeptidase II - genetics | Schizophrenia - genetics | Methylenetetrahydrofolate Reductase (NADPH2) - genetics | Ferredoxin-NADP Reductase - genetics | Folic Acid - blood | 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase - genetics | Folic Acid - metabolism | Adult | Female | Polymorphism, Single Nucleotide | Cohort Studies | Regular
genetic risk score | methylation | epigenetics | gene-environment interaction | BLADDER-CANCER | DEPRESSION | PSYCHIATRY | COMMON MUTATION | DNA-METHYLATION | METHYLENETETRAHYDROFOLATE REDUCTASE | HOMOCYSTEINE LEVELS | CATECHOL-O-METHYLTRANSFERASE | POLYMORPHISMS | RISK-FACTOR | ONE-CARBON METABOLISM | Severity of Illness Index | Genetic Predisposition to Disease | Schizophrenia - metabolism | Gene Frequency | Humans | Reduced Folate Carrier Protein - genetics | Linear Models | Male | Mutation, Missense | Catechol O-Methyltransferase - genetics | Schizophrenic Psychology | Metabolic Networks and Pathways - genetics | Glutamate Carboxypeptidase II - genetics | Schizophrenia - genetics | Methylenetetrahydrofolate Reductase (NADPH2) - genetics | Ferredoxin-NADP Reductase - genetics | Folic Acid - blood | 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase - genetics | Folic Acid - metabolism | Adult | Female | Polymorphism, Single Nucleotide | Cohort Studies | Regular
Journal Article
Brain Research, ISSN 0006-8993, 2017, Volume 1667, pp. 74 - 83
Highlights • Mitochondria are the organelles responsible for most energy production in the nervous system. • Amyotrophic lateral sclerosis (ALS) is a typically...
Neurology | RNA expression | ALS | TFAM | Mitochondria | Genomics | OXIDATIVE-PHOSPHORYLATION | STEM-CELLS | TOXICITY | CEREBROSPINAL-FLUID | C9ORF72 | NEUROSCIENCES | SPORADIC ALS | BIOGENESIS | EXPANSION | DYSFUNCTION | BRAIN | Recombinant Proteins - metabolism | Transcription Factors - administration & dosage | Brain - diagnostic imaging | Gene Expression | Mitochondrial Proteins - administration & dosage | Humans | Cells, Cultured | Laser Capture Microdissection | DNA, Mitochondrial | Male | Rats, Sprague-Dawley | Recombinant Proteins - administration & dosage | Brain - metabolism | DNA-Binding Proteins - metabolism | Motor Neurons - metabolism | Transcription Factors - metabolism | Animals | Sequence Analysis, RNA | Mitochondrial Proteins - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Cervical Cord - metabolism | DNA-Binding Proteins - administration & dosage | Glucose - metabolism | Neural Stem Cells - metabolism | Amyotrophic lateral sclerosis | Mitochondrial DNA | RNA | Neurons | Analysis | Genes | Nervous system diseases | Genetic research | Genetic transcription
Neurology | RNA expression | ALS | TFAM | Mitochondria | Genomics | OXIDATIVE-PHOSPHORYLATION | STEM-CELLS | TOXICITY | CEREBROSPINAL-FLUID | C9ORF72 | NEUROSCIENCES | SPORADIC ALS | BIOGENESIS | EXPANSION | DYSFUNCTION | BRAIN | Recombinant Proteins - metabolism | Transcription Factors - administration & dosage | Brain - diagnostic imaging | Gene Expression | Mitochondrial Proteins - administration & dosage | Humans | Cells, Cultured | Laser Capture Microdissection | DNA, Mitochondrial | Male | Rats, Sprague-Dawley | Recombinant Proteins - administration & dosage | Brain - metabolism | DNA-Binding Proteins - metabolism | Motor Neurons - metabolism | Transcription Factors - metabolism | Animals | Sequence Analysis, RNA | Mitochondrial Proteins - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Cervical Cord - metabolism | DNA-Binding Proteins - administration & dosage | Glucose - metabolism | Neural Stem Cells - metabolism | Amyotrophic lateral sclerosis | Mitochondrial DNA | RNA | Neurons | Analysis | Genes | Nervous system diseases | Genetic research | Genetic transcription
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2011, Volume 6, Issue 9, p. e25253
Background: Responding to errors is a critical first step in learning from mistakes, a process that is abnormal in schizophrenia. To gain insight into the...
METHYLENETETRAHYDROFOLATE REDUCTASE | EXECUTIVE FUNCTION | HUMAN CEREBRAL-CORTEX | POLYMORPHISMS | PERFORMANCE | ANTERIOR CINGULATE | BIOLOGY | NEURONS | DISORDERS | COMMON MUTATION | DNA-METHYLATION | Magnetic Resonance Imaging | Genetic Predisposition to Disease | Schizophrenia - genetics | Methylenetetrahydrofolate Reductase (NADPH2) - genetics | Humans | Alleles | Adult | Female | Male | DNA Methylation - genetics | Methylenetetrahydrofolate Reductase (NADPH2) - metabolism | Schizophrenia | Methylation | Epigenetic inheritance | Mental disorders | Pathogenesis | Genes | Colorectal cancer | Cognitive ability | Activation | Methylenetetrahydrofolate reductase | Medical schools | Psychosis | Human error | Vitamin B | DNA methylation | Functional magnetic resonance imaging | Deoxyribonucleic acid--DNA | Cortex (cingulate) | Dopamine | Metabolism | Patients | Carbon | Genetic variance | Errors | Saccadic eye movements | Molecular modelling | Epigenetics | Protein expression | Homocysteine | Psychiatry | Deoxyribonucleic acid | DNA
METHYLENETETRAHYDROFOLATE REDUCTASE | EXECUTIVE FUNCTION | HUMAN CEREBRAL-CORTEX | POLYMORPHISMS | PERFORMANCE | ANTERIOR CINGULATE | BIOLOGY | NEURONS | DISORDERS | COMMON MUTATION | DNA-METHYLATION | Magnetic Resonance Imaging | Genetic Predisposition to Disease | Schizophrenia - genetics | Methylenetetrahydrofolate Reductase (NADPH2) - genetics | Humans | Alleles | Adult | Female | Male | DNA Methylation - genetics | Methylenetetrahydrofolate Reductase (NADPH2) - metabolism | Schizophrenia | Methylation | Epigenetic inheritance | Mental disorders | Pathogenesis | Genes | Colorectal cancer | Cognitive ability | Activation | Methylenetetrahydrofolate reductase | Medical schools | Psychosis | Human error | Vitamin B | DNA methylation | Functional magnetic resonance imaging | Deoxyribonucleic acid--DNA | Cortex (cingulate) | Dopamine | Metabolism | Patients | Carbon | Genetic variance | Errors | Saccadic eye movements | Molecular modelling | Epigenetics | Protein expression | Homocysteine | Psychiatry | Deoxyribonucleic acid | DNA
Journal Article