ULTRASTRUCTURAL STUDIES IN ALZHEIMER'S PRESENILE DEMENTIA.
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Alzheimer's disease as homeostatic responses to age-related myelin breakdownAmyloids: friend or foe?Presenilin binding protein is associated with neurofibrillary alterations in Alzheimer's disease and stimulates tau phosphorylationVascular consequences of passive Abeta immunization for Alzheimer's disease. Is avoidance of "malactivation" of microglia enough?Multi-Target Directed Donepezil-Like Ligands for Alzheimer's DiseaseMechanisms of amyloid formation revealed by solution NMRCaenorhabditis elegans as a model organism to study APP functionPreclinical Alzheimer disease: identification of cases at risk among cognitively intact older individualsDo Microglia Default on Network Maintenance in Alzheimer's Disease?Isolation and chemical characterization of Alzheimer's disease paired helical filament cytoskeletons: differentiation from amyloid plaque core proteinMicrotubule-associated protein tau (tau) is a major antigenic component of paired helical filaments in Alzheimer diseaseNoradrenergic Modulation of Cognition in Health and Disease.Amyloid precursor protein-induced axonopathies are independent of amyloid-beta peptides.An electron microscopic and radioautographic study on experimental kernicterus. II. Bilirubin movement within neurons and release of waste products via astroglia.Altered synaptic terminals in cortex near tumorExpression in cultured human neuroblastoma cells of epitopes associated with affected neurons in Alzheimer's disease.Casein kinase II alteration precedes tau accumulation in tangle formationAmyloid angiopathy and lobar cerebral haemorrhage.Pericellular innervation of neurons expressing abnormally hyperphosphorylated tau in the hippocampal formation of Alzheimer's disease patients.Laminar-specific distribution and infrastructural detail of amyloid in the Alzheimer disease cortex visualized by computer-enhanced imaging of epitopes recognized by monoclonal antibodies.Effects of heparin and enoxaparin on APP processing and Aβ production in primary cortical neurons from Tg2576 mice.Proliferation in the Alzheimer hippocampus is due to microglia, not astroglia, and occurs at sites of amyloid deposition.PART, a distinct tauopathy, different from classical sporadic Alzheimer disease.Defective macroautophagic turnover of brain lipids in the TgCRND8 Alzheimer mouse model: prevention by correcting lysosomal proteolytic deficits.Insulin-resistant brain state: the culprit in sporadic Alzheimer's disease?Link between DYRK1A overexpression and several-fold enhancement of neurofibrillary degeneration with 3-repeat tau protein in Down syndromeAmyloid-beta induced CA1 pyramidal cell loss in young adult rats is alleviated by systemic treatment with FGL, a neural cell adhesion molecule-derived mimetic peptide.Induction of intracellular tau aggregation is promoted by α-synuclein seeds and provides novel insights into the hyperphosphorylation of tau.Hook proteins: association with Alzheimer pathology and regulatory role of hook3 in amyloid beta generationA rational approach to dementiaHistoric evidence to support a causal relationship between spirochetal infections and Alzheimer's disease.Role of abnormally phosphorylated tau in the breakdown of microtubules in Alzheimer diseaseMyelin basic protein associates with AβPP, Aβ1-42, and amyloid plaques in cortex of Alzheimer's disease brainPotential natural products for Alzheimer's disease: targeted search using the internal ribosome entry site of tau and amyloid-β precursor protein.Purification, ultrastructure, and chemical analysis of Alzheimer disease amyloid plaque core protein.Investigating how peptide length and a pathogenic mutation modify the structural ensemble of amyloid beta monomer.In Alzheimer's disease the Golgi apparatus of a population of neurons without neurofibrillary tangles is fragmented and atrophic.Association of microglia with amyloid plaques in brains of APP23 transgenic mice.Atomic force microscopy of paired helical filaments isolated from the autopsied brains of patients with Alzheimer's disease and immunolabeled against microtubule-associated protein tau.Diffuse plaques do not accentuate synapse loss in Alzheimer's disease.
P2860
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P2860
ULTRASTRUCTURAL STUDIES IN ALZHEIMER'S PRESENILE DEMENTIA.
description
1964 nî lūn-bûn
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1964年の論文
@ja
1964年論文
@yue
1964年論文
@zh-hant
1964年論文
@zh-hk
1964年論文
@zh-mo
1964年論文
@zh-tw
1964年论文
@wuu
1964年论文
@zh
1964年论文
@zh-cn
name
ULTRASTRUCTURAL STUDIES IN ALZHEIMER'S PRESENILE DEMENTIA.
@ast
ULTRASTRUCTURAL STUDIES IN ALZHEIMER'S PRESENILE DEMENTIA.
@en
type
label
ULTRASTRUCTURAL STUDIES IN ALZHEIMER'S PRESENILE DEMENTIA.
@ast
ULTRASTRUCTURAL STUDIES IN ALZHEIMER'S PRESENILE DEMENTIA.
@en
prefLabel
ULTRASTRUCTURAL STUDIES IN ALZHEIMER'S PRESENILE DEMENTIA.
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ULTRASTRUCTURAL STUDIES IN ALZHEIMER'S PRESENILE DEMENTIA.
@en
P2093
P2860
P1476
ULTRASTRUCTURAL STUDIES IN ALZHEIMER'S PRESENILE DEMENTIA.
@en
P2093
P2860
P304
P407
P577
1964-02-01T00:00:00Z