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).
about
The generation and function of soluble apoE receptors in the CNSIn vivo imaging reveals sigmoidal growth kinetic of β-amyloid plaques.Aggregation and disaggregation of senile plaques in Alzheimer diseaseA genetic cause of Alzheimer disease: mechanistic insights from Down syndromeCytoskeletal pathologies of Alzheimer diseaseInteractions dominate the dynamics of visual cognition.Biochemical and immunohistochemical analysis of an Alzheimer's disease mouse model reveals the presence of multiple cerebral Abeta assembly forms throughout life.Deficient high-affinity binding of Pittsburgh compound B in a case of Alzheimer's diseaseQuantification of amyloid precursor protein isoforms using quantification concatamer internal standard.Size frequency distribution of the beta-amyloid (abeta) deposits in dementia with Lewy bodies with associated Alzheimer's disease pathologyQuantification of Butyrylcholinesterase Activity as a Sensitive and Specific Biomarker of Alzheimer's Disease.Astrocyte lipoproteins, effects of apoE on neuronal function, and role of apoE in amyloid-beta deposition in vivo.Dynamics of plaque formation in Alzheimer's disease.Neurotoxic effects of thioflavin S-positive amyloid deposits in transgenic mice and Alzheimer's disease.Alzheimer diseases: a model of gene mutations and susceptibility polymorphisms for complex psychiatric diseases.Genetic analysis of contributions of dorsal group and JAK-Stat92E pathway genes to larval hemocyte concentration and the egg encapsulation response in Drosophila.Pittsburgh compound B (11C-PIB) and fluorodeoxyglucose (18 F-FDG) PET in patients with Alzheimer disease, mild cognitive impairment, and healthy controlsAPOEε2 is associated with milder clinical and pathological Alzheimer disease.Rapid appearance and local toxicity of amyloid-beta plaques in a mouse model of Alzheimer's diseaseCerebral lipid deposition in aged apolipoprotein-E-deficient mice.Stable size distribution of amyloid plaques over the course of Alzheimer disease.Orchestrated experience-driven Arc responses are disrupted in a mouse model of Alzheimer's disease.Neuropathologically defined subtypes of Alzheimer's disease differ significantly from neurofibrillary tangle-predominant dementia.Apolipoprotein E is essential for amyloid deposition in the APP(V717F) transgenic mouse model of Alzheimer's diseaseDifferential relationships of reactive astrocytes and microglia to fibrillar amyloid deposits in Alzheimer disease.The apolipoprotein E allele epsilon 4 does not correlate with the number of senile plaques or neurofibrillary tangles in patients with Alzheimer's disease.Imaging Alzheimer pathology in late-life depression with PET and Pittsburgh Compound-BLabel-free optical quantification of structural alterations in Alzheimer's diseaseAnti-LRP/LR specific antibody IgG1-iS18 and knock-down of LRP/LR by shRNAs rescue cells from Aβ42 induced cytotoxicityLarge Soluble Oligomers of Amyloid β-Protein from Alzheimer Brain Are Far Less Neuroactive Than the Smaller Oligomers to Which They Dissociate.On the nucleation and growth of amyloid beta-protein fibrils: detection of nuclei and quantitation of rate constants.Apolipoprotein E in Alzheimer's disease and other neurological disorders.Neurotoxicity of amyloid β-protein: synaptic and network dysfunction.Mouse-based genetic modeling and analysis of Down syndrome.Biostatistical analysis of quantitative immunofluorescence microscopy images.Clinical and neuropathological correlates of apolipoprotein E genotype in Alzheimer's disease. Window on molecular epidemiology.Amyloid beta-protein and the genetics of Alzheimer's disease.Homocysteine and related genetic polymorphisms in Down's syndrome IQ.Spectroscopic imaging with spectral domain visible light optical coherence microscopy in Alzheimer's disease brain samples.Cellular source of apolipoprotein E4 determines neuronal susceptibility to excitotoxic injury in transgenic mice
P2860
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P2860
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).
description
1995 nî lūn-bûn
@nan
1995 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
1995 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
1995年の論文
@ja
1995年論文
@yue
1995年論文
@zh-hant
1995年論文
@zh-hk
1995年論文
@zh-mo
1995年論文
@zh-tw
1995年论文
@wuu
name
Quantitative analysis of senil ...... nd trisomy 21 (Down syndrome).
@ast
Quantitative analysis of senil ...... nd trisomy 21 (Down syndrome).
@en
Quantitative analysis of senil ...... tein E genotype and trisomy 21
@nl
type
label
Quantitative analysis of senil ...... nd trisomy 21 (Down syndrome).
@ast
Quantitative analysis of senil ...... nd trisomy 21 (Down syndrome).
@en
Quantitative analysis of senil ...... tein E genotype and trisomy 21
@nl
prefLabel
Quantitative analysis of senil ...... nd trisomy 21 (Down syndrome).
@ast
Quantitative analysis of senil ...... nd trisomy 21 (Down syndrome).
@en
Quantitative analysis of senil ...... tein E genotype and trisomy 21
@nl
P2093
P2860
P50
P356
P1476
Quantitative analysis of senil ...... nd trisomy 21 (Down syndrome).
@en
P2093
P2860
P304
P356
10.1073/PNAS.92.8.3586
P407
P577
1995-04-01T00:00:00Z