Neurotoxic effects of thioflavin S-positive amyloid deposits in transgenic mice and Alzheimer's disease. - Wikidata - awgldk - TriplyDB

Neurotoxic effects of thioflavin S-positive amyloid deposits in transgenic mice and Alzheimer's disease.

Neurotoxic effects of thioflavin S-positive amyloid deposits in transgenic mice and Alzheimer's disease.

http://www.wikidata.org/entity/Q34391393

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Protein phosphatase 5 protects neurons against amyloid-beta toxicity Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer's disease Neuropathological alterations in Alzheimer disease Amyloid-associated activity contributes to the severity and toxicity of a prion phenotype Massive CA1/2 neuronal loss with intraneuronal and N-terminal truncated Abeta42 accumulation in a novel Alzheimer transgenic model Alzheimer disease models and human neuropathology: similarities and differences Neuron recognition by parallel Potts segmentation.Biophysics of Parkinson's disease: structure and aggregation of alpha-synuclein.Dendritic vulnerability in neurodegenerative disease: insights from analyses of cortical pyramidal neurons in transgenic mouse models A computational model for the loss of neuronal organization in microcolumns Transgenic models of Alzheimer's disease: learning from animals PI3 kinase signaling is involved in Abeta-induced memory loss in Drosophila.Neuronal and axonal loss are selectively linked to fibrillar amyloid-{beta} within plaques of the aged primate cerebral cortex.The intersection of amyloid beta and tau at synapses in Alzheimer's disease Neuron loss in transgenic mouse models of Alzheimer's disease Diversity-driven chemical probe development for biomolecules: beyond hypothesis-driven approach.Probing the biology of Alzheimer's disease in mice.Antioxidants have a rapid and long-lasting effect on neuritic abnormalities in APP:PS1 mice.The absence of myelin basic protein promotes neuroinflammation and reduces amyloid β-protein accumulation in Tg-5xFAD mice.Recommendations for Development of New Standardized Forms of Cocoa Breeds and Cocoa Extract Processing for the Prevention of Alzheimer's Disease: Role of Cocoa in Promotion of Cognitive Resilience and Healthy Brain Aging.Age-related reduction in microcolumnar structure in area 46 of the rhesus monkey correlates with behavioral decline Generating a model of the three-dimensional spatial distribution of neurons using density maps.Early fear memory defects are associated with altered synaptic plasticity and molecular architecture in the TgCRND8 Alzheimer's disease mouse model.The amyloid beta ion channel hypothesis of Alzheimer's disease.Abeta42-driven cerebral amyloidosis in transgenic mice reveals early and robust pathology.N-terminal region of myelin basic protein reduces fibrillar amyloid-β deposition in Tg-5xFAD mice.Dense-core plaques in Tg2576 and PSAPP mouse models of Alzheimer's disease are centered on vessel walls A welcoming environment for amyloid plaques.Increased T cell reactivity to amyloid beta protein in older humans and patients with Alzheimer disease Characterization of a Novel Mouse Model of Alzheimer's Disease--Amyloid Pathology and Unique β-Amyloid Oligomer Profile.BACE1 gene deletion prevents neuron loss and memory deficits in 5XFAD APP/PS1 transgenic mice Neuronal structure is altered by amyloid plaques.Cerebral microvascular rather than parenchymal amyloid-β protein pathology promotes early cognitive impairment in transgenic mice Orchestrated experience-driven Arc responses are disrupted in a mouse model of Alzheimer's disease.Topological analyses in APP/PS1 mice reveal that astrocytes do not migrate to amyloid-β plaques.Nanoimaging for protein misfolding and related diseases.Two-photon imaging of synaptic plasticity and pathology in the living mouse brain.Nanotools for megaproblems: probing protein misfolding diseases using nanomedicine modus operandi Involvement of perineuronal and perisynaptic extracellular matrix in Alzheimer's disease neuropathology Fine mapping of the amyloid β-protein binding site on myelin basic protein.

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Neurotoxic effects of thioflavin S-positive amyloid deposits in transgenic mice and Alzheimer's disease.

http://www.wikidata.org/entity/Q34391393

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2002 nî lūn-bûn

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2002 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2002年の論文

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Neurotoxic effects of thioflav ...... mice and Alzheimer's disease.

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Neurotoxic effects of thioflav ...... mice and Alzheimer's disease.

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Proceedings of the National Academy of Sciences of the United States of America

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Neurotoxic effects of thioflav ...... mice and Alzheimer's disease.

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B T Hyman

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J Sanders

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K Duff

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K Hsiao Ashe

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M C Irizarry

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P2860

Correlative Memory Deficits, Abeta Elevation, and Amyloid Plaques in Transgenic Mice

Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides

Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1

Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease

Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease

Mutation of the beta-amyloid precursor protein in familial Alzheimer's disease increases beta-protein production.

Quantitative analysis of senile plaques in Alzheimer disease: observation of log-normal size distribution and molecular epidemiology of differences associated with apolipoprotein E genotype and trisomy 21 (Down syndrome).

Methodological variables in the assessment of beta amyloid neurotoxicity.

Age-related amyloid beta deposition in transgenic mice overexpressing both Alzheimer mutant presenilin 1 and amyloid beta precursor protein Swedish mutant is not associated with global neuronal loss.

Beta-amyloid neurotoxicity requires fibril formation and is inhibited by congo red.

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13990-13995

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10.1073/PNAS.222433299

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Harry Eugene Stanley

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11084885

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12374847

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Alzheimer's disease

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