Diffuse senile plaques occur commonly in the cerebellum in Alzheimer's disease.
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Contribution by synaptic zinc to the gender-disparate plaque formation in human Swedish mutant APP transgenic miceMR-less surface-based amyloid assessment based on 11C PiB PETMoving forward: age effects on the cerebellum underlie cognitive and motor declinesTransgenic mice overexpressing reticulon 3 develop neuritic abnormalities.A semi-automated workflow solution for multimodal neuroimaging: application to patients with traumatic brain injury.Identification of valid reference genes for the normalization of RT qPCR gene expression data in human brain tissueMicroglial activation and amyloid deposition in mild cognitive impairment: a PET studyQuantitative analysis of [18F]FDDNP PET using subcortical white matter as reference regionSelective Transgenic Expression of Mutant Ubiquitin in Purkinje Cell Stripes in the Cerebellum.Increased metabolic vulnerability in early-onset Alzheimer's disease is not related to amyloid burdenComparisons of telomere lengths in peripheral blood and cerebellum in Alzheimer's disease.DNA damage and cell cycle events implicate cerebellar dentate nucleus neurons as targets of Alzheimer's disease.Pathology associated with AAV mediated expression of beta amyloid or C100 in adult mouse hippocampus and cerebellumNeuropathological and biochemical assessments of an Alzheimer's disease patient treated with the γ-secretase inhibitor semagacestat.Voxel-based analysis of 11C-PIB scans for diagnosing Alzheimer's disease.Pittsburgh compound B (11C-PIB) and fluorodeoxyglucose (18 F-FDG) PET in patients with Alzheimer disease, mild cognitive impairment, and healthy controlsSecretory PLA2-IIA: a new inflammatory factor for Alzheimer's disease.Plasma Aβ and PET PiB binding are inversely related in mild cognitive impairment.Clinicopathologic and 11C-Pittsburgh compound B implications of Thal amyloid phase across the Alzheimer's disease spectrum.Amyloid deposition begins in the striatum of presenilin-1 mutation carriers from two unrelated pedigreesDiffuse plaques do not accentuate synapse loss in Alzheimer's disease.Molecular features of hypothalamic plaques in Alzheimer's disease.Heparan sulfate proteoglycan in diffuse plaques of hippocampus but not of cerebellum in Alzheimer's disease brain.Expression of the low-affinity nerve growth factor receptor enhances beta-amyloid peptide toxicity.Reference tissue normalization in longitudinal (18)F-florbetapir positron emission tomography of late mild cognitive impairment.Impact of amyloid imaging on drug development in Alzheimer's disease.Amyloid beta-protein as a substrate interacts with extracellular matrix to promote neurite outgrowthCaspase-cleaved glial fibrillary acidic protein within cerebellar white matter of the Alzheimer's disease brainExpression profiles of cytokines in the brains of Alzheimer's disease (AD) patients compared to the brains of non-demented patients with and without increasing AD pathology.Neurons in Vulnerable Regions of the Alzheimer's Disease Brain Display Reduced ATM Signaling.A transgenic Alzheimer rat with plaques, tau pathology, behavioral impairment, oligomeric aβ, and frank neuronal lossRegional analysis of FDG and PIB-PET images in normal aging, mild cognitive impairment, and Alzheimer's diseaseReduced amyloid deposition in mice overexpressing RTN3 is adversely affected by preformed dystrophic neurites.Comparative evaluation of Logan and relative-equilibrium graphical methods for parametric imaging of dynamic [18F]FDDNP PET determinationsTest-retest variability of quantitative [11C]PIB studies in Alzheimer's disease.Molecular pathogenesis of Alzheimer's disease: reductionist versus expansionist approaches.Glial cytokines in Alzheimer's disease: review and pathogenic implicationsDefined neurofilament, tau, and beta-amyloid precursor protein epitopes distinguish Alzheimer from non-Alzheimer senile plaques.Cytokines and Cytokine Receptors Involved in the Pathogenesis of Alzheimer's Disease.Regulatory region of human amyloid precursor protein (APP) gene promotes neuron-specific gene expression in the CNS of transgenic mice.
P2860
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P2860
Diffuse senile plaques occur commonly in the cerebellum in Alzheimer's disease.
description
1989 nî lūn-bûn
@nan
1989年の論文
@ja
1989年論文
@yue
1989年論文
@zh-hant
1989年論文
@zh-hk
1989年論文
@zh-mo
1989年論文
@zh-tw
1989年论文
@wuu
1989年论文
@zh
1989年论文
@zh-cn
name
Diffuse senile plaques occur commonly in the cerebellum in Alzheimer's disease.
@ast
Diffuse senile plaques occur commonly in the cerebellum in Alzheimer's disease.
@en
type
label
Diffuse senile plaques occur commonly in the cerebellum in Alzheimer's disease.
@ast
Diffuse senile plaques occur commonly in the cerebellum in Alzheimer's disease.
@en
prefLabel
Diffuse senile plaques occur commonly in the cerebellum in Alzheimer's disease.
@ast
Diffuse senile plaques occur commonly in the cerebellum in Alzheimer's disease.
@en
P2093
P2860
P1476
Diffuse senile plaques occur commonly in the cerebellum in Alzheimer's disease.
@en
P2093
C L Joachim
D J Selkoe
J H Morris
P2860
P304
P407
P577
1989-08-01T00:00:00Z