Acta Neuropathologica, ISSN 0001-6322, 2/2018, Volume 135, Issue 2, pp. 201 - 212
Abeta deposits and tau pathology were investigated in 24 French patients that died from iatrogenic Creutzfeldt–Jakob disease after exposure to cadaver-derived...
Pathology | Neurosciences | Medicine & Public Health | Alzheimer’s disease | Prions | Transmission | Tau pathology | Growth hormone | Creutzfeldt–Jakob disease | Abeta pathology | TAU-PROTEIN | ALZHEIMER BRAIN | Creutzfeldt-Jakob disease | PATHOLOGY | CEREBROSPINAL-FLUID | NEUROSCIENCES | LESIONS | CLINICAL NEUROLOGY | Alzheimer's disease | AGE | Medicine, Experimental | Medical research | Somatotropin | Medical errors | Analysis | Deposits | Neurodegenerative diseases | Tau protein | Contaminants | Growth hormones | Life Sciences
Pathology | Neurosciences | Medicine & Public Health | Alzheimer’s disease | Prions | Transmission | Tau pathology | Growth hormone | Creutzfeldt–Jakob disease | Abeta pathology | TAU-PROTEIN | ALZHEIMER BRAIN | Creutzfeldt-Jakob disease | PATHOLOGY | CEREBROSPINAL-FLUID | NEUROSCIENCES | LESIONS | CLINICAL NEUROLOGY | Alzheimer's disease | AGE | Medicine, Experimental | Medical research | Somatotropin | Medical errors | Analysis | Deposits | Neurodegenerative diseases | Tau protein | Contaminants | Growth hormones | Life Sciences
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2017, Volume 12, Issue 2, p. e0172428
The transmission of classical bovine spongiform encephalopathy (C-BSE) through contaminated meat product consumption is responsible for variant...
SCRAPIE | TRANSMISSIBLE MINK ENCEPHALOPATHY | MULTIDISCIPLINARY SCIENCES | PRP TRANSGENIC MICE | SHEEP | CREUTZFELDT-JAKOB-DISEASE | CEREBROSPINAL-FLUID | INTERSPECIES TRANSMISSION | BSE TRANSMISSION | STRAIN | HUMAN PRION PROTEIN | Prion Proteins - analysis | Recombinant Proteins - analysis | Humans | Encephalopathy, Bovine Spongiform - diagnosis | Creutzfeldt-Jakob Syndrome - veterinary | Creutzfeldt-Jakob Syndrome - diagnosis | Animals | Cattle | Sensitivity and Specificity | Primate Diseases - diagnosis | Brain - pathology | Creutzfeldt-Jakob Syndrome - pathology | Brain Chemistry | Encephalopathy, Bovine Spongiform - pathology | Primates | Research | Analysis | Bovine spongiform encephalopathy | Risk factors | Epidemics | Creutzfeldt-Jakob disease | Homology | Assaying | Meat | Proteins | BSE | Transgenic animals | Encephalopathy | Rodents | Prion protein | Public health | Transgenic mice | Real time | Conversion | Virology | Studies | Infectious diseases | Brain research | Discrimination | Surveillance | Prions
SCRAPIE | TRANSMISSIBLE MINK ENCEPHALOPATHY | MULTIDISCIPLINARY SCIENCES | PRP TRANSGENIC MICE | SHEEP | CREUTZFELDT-JAKOB-DISEASE | CEREBROSPINAL-FLUID | INTERSPECIES TRANSMISSION | BSE TRANSMISSION | STRAIN | HUMAN PRION PROTEIN | Prion Proteins - analysis | Recombinant Proteins - analysis | Humans | Encephalopathy, Bovine Spongiform - diagnosis | Creutzfeldt-Jakob Syndrome - veterinary | Creutzfeldt-Jakob Syndrome - diagnosis | Animals | Cattle | Sensitivity and Specificity | Primate Diseases - diagnosis | Brain - pathology | Creutzfeldt-Jakob Syndrome - pathology | Brain Chemistry | Encephalopathy, Bovine Spongiform - pathology | Primates | Research | Analysis | Bovine spongiform encephalopathy | Risk factors | Epidemics | Creutzfeldt-Jakob disease | Homology | Assaying | Meat | Proteins | BSE | Transgenic animals | Encephalopathy | Rodents | Prion protein | Public health | Transgenic mice | Real time | Conversion | Virology | Studies | Infectious diseases | Brain research | Discrimination | Surveillance | Prions
Journal Article
Brain, ISSN 0006-8950, 2017, Volume 140, Issue 1, pp. 184 - 200
Alzheimer's disease is characterized by the combined presence of amyloid plaques and tau pathology, the latter being correlated with the progression of...
Frontotemporal lobar degeneration | Neuroinflammation | T cells | Tauopathy | Chemokines | tauopathy | MICROGLIAL ACTIVATION | ALZHEIMERS-DISEASE | SYNAPTIC-TRANSMISSION | PATHOLOGY | chemokines | BLOOD-BRAIN-BARRIER | NEUROSCIENCES | CLINICAL NEUROLOGY | IMMUNE-SYSTEM | neuroinflammation | TAU TRANSGENIC MOUSE | LONG-TERM DEPRESSION | A-BETA | CENTRAL-NERVOUS-SYSTEM | frontotemporal lobar degeneration | Antibodies - therapeutic use | Hippocampus - immunology | Tauopathies - immunology | Humans | Mice, Inbred C57BL | Middle Aged | Mice, Transgenic | Inflammation - immunology | CD4-Positive T-Lymphocytes - immunology | Inflammation - therapy | Animals | Cognitive Dysfunction - immunology | Cerebral Cortex - immunology | CD3 Complex - immunology | Cognitive Dysfunction - therapy | Tauopathies - therapy | Aged | Mice | CD8-Positive T-Lymphocytes - immunology | Chemokines - immunology | Disease Models, Animal | Life Sciences | Neurons and Cognition | Original | 1060
Frontotemporal lobar degeneration | Neuroinflammation | T cells | Tauopathy | Chemokines | tauopathy | MICROGLIAL ACTIVATION | ALZHEIMERS-DISEASE | SYNAPTIC-TRANSMISSION | PATHOLOGY | chemokines | BLOOD-BRAIN-BARRIER | NEUROSCIENCES | CLINICAL NEUROLOGY | IMMUNE-SYSTEM | neuroinflammation | TAU TRANSGENIC MOUSE | LONG-TERM DEPRESSION | A-BETA | CENTRAL-NERVOUS-SYSTEM | frontotemporal lobar degeneration | Antibodies - therapeutic use | Hippocampus - immunology | Tauopathies - immunology | Humans | Mice, Inbred C57BL | Middle Aged | Mice, Transgenic | Inflammation - immunology | CD4-Positive T-Lymphocytes - immunology | Inflammation - therapy | Animals | Cognitive Dysfunction - immunology | Cerebral Cortex - immunology | CD3 Complex - immunology | Cognitive Dysfunction - therapy | Tauopathies - therapy | Aged | Mice | CD8-Positive T-Lymphocytes - immunology | Chemokines - immunology | Disease Models, Animal | Life Sciences | Neurons and Cognition | Original | 1060
Journal Article
Molecular Psychiatry, ISSN 1359-4184, 01/2019, Volume 24, Issue 1, pp. 108 - 125
Extracellular aggregates of amyloid β (Aβ) peptides, which are characteristic of Alzheimer’s disease (AD), act as an essential trigger for glial cell...
Amyloidogenesis | Neuroprotection | Peptides | Therapeutic applications | Purine receptors | CD8 antigen | Transgenic mice | Cognitive ability | CCL3 protein | Lymphocytes T | Inflammation | IL-1β | Amyloid precursor protein | Proteins | Receptors | Cell activation | Plasticity (synaptic) | Lymphocytes | Mice | Lesions | Alzheimer's disease | Chemokines | Neuroscience | Physiology | Diseases
Amyloidogenesis | Neuroprotection | Peptides | Therapeutic applications | Purine receptors | CD8 antigen | Transgenic mice | Cognitive ability | CCL3 protein | Lymphocytes T | Inflammation | IL-1β | Amyloid precursor protein | Proteins | Receptors | Cell activation | Plasticity (synaptic) | Lymphocytes | Mice | Lesions | Alzheimer's disease | Chemokines | Neuroscience | Physiology | Diseases
Journal Article
Acta Neuropathologica, ISSN 0001-6322, 4/2013, Volume 125, Issue 4, pp. 511 - 522
Mutations in SQSTM1 encoding the sequestosome 1/p62 protein have recently been identified in familial and sporadic cases of amyotrophic lateral sclerosis...
Pathology | Neurosciences | Medicine & Public Health | Neuropathology | Motor neuron disease | Paget’s disease | FTLD–ALS | p62 | Familial and sporadic ALS | FTLD-ALS | Paget's disease | DOMAIN | UBIQUITIN-BINDING | BINDING PROTEIN P62 | TDP-43 PATHOLOGY | ALS PATIENTS | PATHOLOGY | FRONTOTEMPORAL LOBAR DEGENERATION | C9ORF72 | NEUROSCIENCES | CLINICAL NEUROLOGY | PAGETS-DISEASE | BONE | HEXANUCLEOTIDE REPEAT | Sequestosome-1 Protein | Amyotrophic Lateral Sclerosis - genetics | Humans | Middle Aged | Ubiquitin - metabolism | Male | Ubiquitin - genetics | DNA-Binding Proteins - genetics | DNA-Binding Proteins - metabolism | Amyotrophic Lateral Sclerosis - pathology | Adaptor Proteins, Signal Transducing - genetics | Aged, 80 and over | Brain - pathology | Adult | Female | Heterozygote | Aged | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Ubiquitin | Amyotrophic lateral sclerosis | Genetic aspects | Gene mutations | Analysis | Genes
Pathology | Neurosciences | Medicine & Public Health | Neuropathology | Motor neuron disease | Paget’s disease | FTLD–ALS | p62 | Familial and sporadic ALS | FTLD-ALS | Paget's disease | DOMAIN | UBIQUITIN-BINDING | BINDING PROTEIN P62 | TDP-43 PATHOLOGY | ALS PATIENTS | PATHOLOGY | FRONTOTEMPORAL LOBAR DEGENERATION | C9ORF72 | NEUROSCIENCES | CLINICAL NEUROLOGY | PAGETS-DISEASE | BONE | HEXANUCLEOTIDE REPEAT | Sequestosome-1 Protein | Amyotrophic Lateral Sclerosis - genetics | Humans | Middle Aged | Ubiquitin - metabolism | Male | Ubiquitin - genetics | DNA-Binding Proteins - genetics | DNA-Binding Proteins - metabolism | Amyotrophic Lateral Sclerosis - pathology | Adaptor Proteins, Signal Transducing - genetics | Aged, 80 and over | Brain - pathology | Adult | Female | Heterozygote | Aged | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Ubiquitin | Amyotrophic lateral sclerosis | Genetic aspects | Gene mutations | Analysis | Genes
Journal Article
MOLECULAR PSYCHIATRY, ISSN 1359-4184, 01/2019, Volume 24, Issue 1, pp. 108 - 125
Extracellular aggregates of amyloid beta (A beta) peptides, which are characteristic of Alzheimer's disease (AD), act as an essential trigger for glial cell...
COMMON VARIANTS | PSYCHIATRY | BIOCHEMISTRY & MOLECULAR BIOLOGY | AMYLOID PLAQUES | NEUROSCIENCES | P2Y NUCLEOTIDE RECEPTORS | MICROGLIA | NEUROINFLAMMATION | PURINERGIC P2X RECEPTOR | APOPTOTIC CELLS | CENTRAL-NERVOUS-SYSTEM | CHEMOKINE RECEPTORS | T-CELLS | Genetic aspects | Rats as laboratory animals | Research | Alzheimer's disease | Chemokines | Life Sciences | Neurons and Cognition | Neurobiology
COMMON VARIANTS | PSYCHIATRY | BIOCHEMISTRY & MOLECULAR BIOLOGY | AMYLOID PLAQUES | NEUROSCIENCES | P2Y NUCLEOTIDE RECEPTORS | MICROGLIA | NEUROINFLAMMATION | PURINERGIC P2X RECEPTOR | APOPTOTIC CELLS | CENTRAL-NERVOUS-SYSTEM | CHEMOKINE RECEPTORS | T-CELLS | Genetic aspects | Rats as laboratory animals | Research | Alzheimer's disease | Chemokines | Life Sciences | Neurons and Cognition | Neurobiology
Journal Article
Acta neuropathologica communications, ISSN 2051-5960, 01/2018, Volume 6, Issue 1, pp. 5 - 19
The presence of pathology related to the deposition of amyloid-beta (A beta) has been recently reported in iatrogenic Creutzfeldt-Jakob disease (iCJD) acquired...
Thioflavin S | Pathology | Cerebral amyloid angiopathy | Amyloid-β | iCJD | MOUSE-BRAIN | DURA-MATER GRAFT | PRION TRANSMISSION | CLASSIFICATION | ALPHA-SYNUCLEIN | RECIPIENTS | NEUROSCIENCES | SEEDS | GROWTH-HORMONE | ANGIOPATHY | ALZHEIMER-TYPE NEUROPATHOLOGY | Amyloid-beta
Thioflavin S | Pathology | Cerebral amyloid angiopathy | Amyloid-β | iCJD | MOUSE-BRAIN | DURA-MATER GRAFT | PRION TRANSMISSION | CLASSIFICATION | ALPHA-SYNUCLEIN | RECIPIENTS | NEUROSCIENCES | SEEDS | GROWTH-HORMONE | ANGIOPATHY | ALZHEIMER-TYPE NEUROPATHOLOGY | Amyloid-beta
Journal Article
Neurobiology of Disease, ISSN 0969-9961, 2015, Volume 94, pp. 32 - 43
Abstract Single nucleotide polymorphisms in PICALM, a key component of clathrin-mediated endocytosis machinery, have been identified as genetic susceptibility...
Neurology | Beclin-1 | FTLD-MAPT | Tau | Pick disease | Autophagy | NFTs | Progressive supranuclear palsy | FTLD-TDP | Alzheimer's disease | Corticobasal degeneration | LC3 | PICALM | Diffuse Lewy body disease | NEUROFIBRILLARY TANGLES | ALZHEIMERS-DISEASE | PATHOLOGY | FRONTOTEMPORAL LOBAR DEGENERATION | NEUROSCIENCES | IDENTIFIES VARIANTS | EXPRESSION | BRAIN | GENOME-WIDE ASSOCIATION | Phosphorylation | Humans | Tauopathies - pathology | tau Proteins - metabolism | Pneumothorax - metabolism | Clathrin - metabolism | Endocytosis - physiology | Brain - metabolism | Neurofibrillary Tangles - metabolism | Frontotemporal Lobar Degeneration - metabolism | Monomeric Clathrin Assembly Proteins - metabolism | Alzheimer Disease - metabolism | Supranuclear Palsy, Progressive - metabolism | Neurons - metabolism | Pick Disease of the Brain - metabolism | Autophagy-Related Proteins - metabolism | Pick's disease | Brain | Clathrin | Nervous system diseases | Computer entertainment systems | Disease susceptibility | Genetic polymorphisms | Life Sciences | Neurons and Cognition | Neurobiology
Neurology | Beclin-1 | FTLD-MAPT | Tau | Pick disease | Autophagy | NFTs | Progressive supranuclear palsy | FTLD-TDP | Alzheimer's disease | Corticobasal degeneration | LC3 | PICALM | Diffuse Lewy body disease | NEUROFIBRILLARY TANGLES | ALZHEIMERS-DISEASE | PATHOLOGY | FRONTOTEMPORAL LOBAR DEGENERATION | NEUROSCIENCES | IDENTIFIES VARIANTS | EXPRESSION | BRAIN | GENOME-WIDE ASSOCIATION | Phosphorylation | Humans | Tauopathies - pathology | tau Proteins - metabolism | Pneumothorax - metabolism | Clathrin - metabolism | Endocytosis - physiology | Brain - metabolism | Neurofibrillary Tangles - metabolism | Frontotemporal Lobar Degeneration - metabolism | Monomeric Clathrin Assembly Proteins - metabolism | Alzheimer Disease - metabolism | Supranuclear Palsy, Progressive - metabolism | Neurons - metabolism | Pick Disease of the Brain - metabolism | Autophagy-Related Proteins - metabolism | Pick's disease | Brain | Clathrin | Nervous system diseases | Computer entertainment systems | Disease susceptibility | Genetic polymorphisms | Life Sciences | Neurons and Cognition | Neurobiology
Journal Article
Acta Neuropathologica, ISSN 0001-6322, 06/2013, Volume 125, Issue 6, pp. 861 - 878
PICALM, a clathrin adaptor protein, plays important roles in clathrin-mediated endocytosis in all cell types. Recently, genome-wide association studies...
Tau | Alzheimer's disease | NFT | Microglia | PICALM | COMMON VARIANTS | GRANULOVACUOLAR DEGENERATION | PATHOLOGY | CASPASE CLEAVAGE | NEUROSCIENCES | CLINICAL NEUROLOGY | ASSEMBLY PROTEIN AP180 | IDENTIFIES VARIANTS | BETA-DEPOSITION | PAIRED HELICAL FILAMENTS | PRECURSOR PROTEIN | MOLECULAR-BASIS | GENOME-WIDE ASSOCIATION | Alzheimer Disease - etiology | Neurofibrillary Tangles - pathology | Down Syndrome - pathology | Down Syndrome - metabolism | Humans | Middle Aged | tau Proteins - metabolism | Male | Down Syndrome - etiology | Case-Control Studies | Alzheimer Disease - pathology | Microglia - physiology | Neurofibrillary Tangles - metabolism | Monomeric Clathrin Assembly Proteins - metabolism | Alzheimer Disease - metabolism | Aged, 80 and over | Adult | Female | Aged
Tau | Alzheimer's disease | NFT | Microglia | PICALM | COMMON VARIANTS | GRANULOVACUOLAR DEGENERATION | PATHOLOGY | CASPASE CLEAVAGE | NEUROSCIENCES | CLINICAL NEUROLOGY | ASSEMBLY PROTEIN AP180 | IDENTIFIES VARIANTS | BETA-DEPOSITION | PAIRED HELICAL FILAMENTS | PRECURSOR PROTEIN | MOLECULAR-BASIS | GENOME-WIDE ASSOCIATION | Alzheimer Disease - etiology | Neurofibrillary Tangles - pathology | Down Syndrome - pathology | Down Syndrome - metabolism | Humans | Middle Aged | tau Proteins - metabolism | Male | Down Syndrome - etiology | Case-Control Studies | Alzheimer Disease - pathology | Microglia - physiology | Neurofibrillary Tangles - metabolism | Monomeric Clathrin Assembly Proteins - metabolism | Alzheimer Disease - metabolism | Aged, 80 and over | Adult | Female | Aged
Journal Article
Molecular Psychiatry, ISSN 1359-4184, 01/2019, Volume 24, Issue 1, pp. 1 - 1
Journal Article
Acta neuropathologica communications, ISSN 2051-5960, 05/2018, Volume 6, Issue 1, pp. 41 - 4
[...]Lewy bodies and 1C2-positive inclusions in substantia nigra, pontine nuclei and cerebellum, described in few parkinsonian patients [9], were absent in our...
Ataxin 2 | GRN | TDP-43 | SCA2 | Amyotrophic lateral sclerosis | Frontotemporal lobar degeneration | Frontotemporal dementia | Corticobasal degeneration | C9orf72 | Corticobasal syndrome | SPINOCEREBELLAR ATAXIA TYPE-2 | PARKINSONISM | ALS | RISK | AMYOTROPHIC-LATERAL-SCLEROSIS | NEUROSCIENCES | REPEAT EXPANSIONS | Frontotemporal Dementia - genetics | Frontotemporal Dementia - diagnostic imaging | Brain - diagnostic imaging | Amyotrophic Lateral Sclerosis - genetics | Humans | Middle Aged | Tomography, Emission-Computed, Single-Photon | Male | Ataxin-2 - genetics | Brain - metabolism | DNA-Binding Proteins - metabolism | Magnetic Resonance Imaging | Aged, 80 and over | Trinucleotide Repeat Expansion - genetics | Female | Aged | Amyotrophic Lateral Sclerosis - diagnostic imaging | Cohort Studies | Neurons | Genes | Dementia | Pathology | Medical imaging | Neuropathology | Ataxia | Mutation | Patients | Life Sciences | Cancer
Ataxin 2 | GRN | TDP-43 | SCA2 | Amyotrophic lateral sclerosis | Frontotemporal lobar degeneration | Frontotemporal dementia | Corticobasal degeneration | C9orf72 | Corticobasal syndrome | SPINOCEREBELLAR ATAXIA TYPE-2 | PARKINSONISM | ALS | RISK | AMYOTROPHIC-LATERAL-SCLEROSIS | NEUROSCIENCES | REPEAT EXPANSIONS | Frontotemporal Dementia - genetics | Frontotemporal Dementia - diagnostic imaging | Brain - diagnostic imaging | Amyotrophic Lateral Sclerosis - genetics | Humans | Middle Aged | Tomography, Emission-Computed, Single-Photon | Male | Ataxin-2 - genetics | Brain - metabolism | DNA-Binding Proteins - metabolism | Magnetic Resonance Imaging | Aged, 80 and over | Trinucleotide Repeat Expansion - genetics | Female | Aged | Amyotrophic Lateral Sclerosis - diagnostic imaging | Cohort Studies | Neurons | Genes | Dementia | Pathology | Medical imaging | Neuropathology | Ataxia | Mutation | Patients | Life Sciences | Cancer
Journal Article
Eurosurveillance, ISSN 1025-496X, 10/2017, Volume 22, Issue 41, pp. 21 - 28
Diagnostic criteria of Creutzfeldt-Jakob disease (CJD), a rare and fatal transmissible nervous system disease with public health implications, are determined...
INFECTIOUS DISEASES | DIFFERENTIAL-DIAGNOSIS | QUAKING-INDUCED CONVERSION | CSF | HUMAN PRION DISEASES | SURVEILLANCE | CODON 129 | TIME | CEREBROSPINAL-FLUID | Brain - diagnostic imaging | Humans | Electroencephalography | Magnetic Resonance Imaging | Creutzfeldt-Jakob Syndrome - diagnosis | Creutzfeldt-Jakob Syndrome - cerebrospinal fluid | 14-3-3 Proteins - cerebrospinal fluid | Autopsy | Prions | Sensitivity and Specificity | Brain - pathology | Female | Prion Proteins - cerebrospinal fluid | Biomarkers - cerebrospinal fluid | Creutzfeldt-Jakob Syndrome - genetics | France | Life Sciences | Santé publique et épidémiologie | Neurons and Cognition | Neurobiology | prion | surveillance | Surveillance and Outbreak Report | biomarkers | Creutzfeldt-Jakob disease | diagnosis criteria
INFECTIOUS DISEASES | DIFFERENTIAL-DIAGNOSIS | QUAKING-INDUCED CONVERSION | CSF | HUMAN PRION DISEASES | SURVEILLANCE | CODON 129 | TIME | CEREBROSPINAL-FLUID | Brain - diagnostic imaging | Humans | Electroencephalography | Magnetic Resonance Imaging | Creutzfeldt-Jakob Syndrome - diagnosis | Creutzfeldt-Jakob Syndrome - cerebrospinal fluid | 14-3-3 Proteins - cerebrospinal fluid | Autopsy | Prions | Sensitivity and Specificity | Brain - pathology | Female | Prion Proteins - cerebrospinal fluid | Biomarkers - cerebrospinal fluid | Creutzfeldt-Jakob Syndrome - genetics | France | Life Sciences | Santé publique et épidémiologie | Neurons and Cognition | Neurobiology | prion | surveillance | Surveillance and Outbreak Report | biomarkers | Creutzfeldt-Jakob disease | diagnosis criteria
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2008, Volume 3, Issue 7, p. e2786
Objective: The glycoprofile of pathological prion protein (PrPres) is widely used as a diagnosis marker in Creutzfeldt-Jakob disease (CJD) and is thought to...
HETEROGENEITY | SPONGIFORM ENCEPHALOPATHIES | PROTEIN | PRPSC | MULTIDISCIPLINARY SCIENCES | MUTATION | PHENOTYPE | SCRAPIE PRION | MOLECULAR-BASIS | BSE AGENT | BRAIN | Brain | Laboratories | Neuropathology | Creutzfeldt-Jakob disease | Glycosylation | Medical diagnosis | Patients | Proteins | BSE | Thalamus | Mutation | Diagnosis | Prion protein | Strains (organisms)
HETEROGENEITY | SPONGIFORM ENCEPHALOPATHIES | PROTEIN | PRPSC | MULTIDISCIPLINARY SCIENCES | MUTATION | PHENOTYPE | SCRAPIE PRION | MOLECULAR-BASIS | BSE AGENT | BRAIN | Brain | Laboratories | Neuropathology | Creutzfeldt-Jakob disease | Glycosylation | Medical diagnosis | Patients | Proteins | BSE | Thalamus | Mutation | Diagnosis | Prion protein | Strains (organisms)
Journal Article
Neurobiology of Aging, ISSN 0197-4580, 2014, Volume 35, Issue 5, pp. 958 - 968
Abstract Caspase cleaved amyloid precursor protein (APPcc) and SET are increased and mislocalized in the neuronal cytoplasm in Alzheimer Disease (AD) brains....
Neurology | Internal Medicine | Caspase cleaved APP | Tau hyperphosphorylation | Down syndrome | SET translocation | Alzheimer disease | Hippocampus | APOPTOSIS | ABNORMAL HYPERPHOSPHORYLATION | PHOSPHORYLATION | TAU | NEUROSCIENCES | CELL-DEATH | GERIATRICS & GERONTOLOGY | DISEASE | ASP664 | PHOSPHATASE-2A | EXPRESSION | MOTONEURONS | Alzheimer Disease - etiology | Caspases - physiology | Phosphorylation | CA1 Region, Hippocampal - cytology | Down Syndrome - metabolism | Humans | Middle Aged | Histone Chaperones - metabolism | tau Proteins - metabolism | Cytoplasm - metabolism | Male | Amyloid beta-Protein Precursor - metabolism | Aged, 80 and over | CA1 Region, Hippocampal - metabolism | Female | Neurons - metabolism | Dentate Gyrus - metabolism | Mice, Inbred C57BL | Disease Progression | Transcription Factors - metabolism | Dentate Gyrus - cytology | Animals | Alzheimer Disease - metabolism | Down Syndrome - genetics | Aged | Mice | Alzheimer Disease - genetics | Brain | Alzheimer's disease | Amyloid beta-protein
Neurology | Internal Medicine | Caspase cleaved APP | Tau hyperphosphorylation | Down syndrome | SET translocation | Alzheimer disease | Hippocampus | APOPTOSIS | ABNORMAL HYPERPHOSPHORYLATION | PHOSPHORYLATION | TAU | NEUROSCIENCES | CELL-DEATH | GERIATRICS & GERONTOLOGY | DISEASE | ASP664 | PHOSPHATASE-2A | EXPRESSION | MOTONEURONS | Alzheimer Disease - etiology | Caspases - physiology | Phosphorylation | CA1 Region, Hippocampal - cytology | Down Syndrome - metabolism | Humans | Middle Aged | Histone Chaperones - metabolism | tau Proteins - metabolism | Cytoplasm - metabolism | Male | Amyloid beta-Protein Precursor - metabolism | Aged, 80 and over | CA1 Region, Hippocampal - metabolism | Female | Neurons - metabolism | Dentate Gyrus - metabolism | Mice, Inbred C57BL | Disease Progression | Transcription Factors - metabolism | Dentate Gyrus - cytology | Animals | Alzheimer Disease - metabolism | Down Syndrome - genetics | Aged | Mice | Alzheimer Disease - genetics | Brain | Alzheimer's disease | Amyloid beta-protein
Journal Article