Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration.
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Neuroprotective effects of physical activity on the brain: a closer look at trophic factor signalingDown syndrome: searching for the genetic culpritsNeurotrophic factors in Alzheimer’s disease: role of axonal transportAlzheimer's disease as homeostatic responses to age-related myelin breakdownProspects for Improving Brain Function in Individuals with Down SyndromeEmerging pharmacotherapies for neurodevelopmental disordersPathogenic mechanisms of a polyglutamine-mediated neurodegenerative disease, spinocerebellar ataxia type 1DYRK1A, a Dosage-Sensitive Gene Involved in Neurodevelopmental Disorders, Is a Target for Drug Development in Down SyndromeThe Roles of Microtubule-Based Transport at Presynaptic Nerve TerminalsDissecting Alzheimer disease in Down syndrome using mouse modelsA genetic cause of Alzheimer disease: mechanistic insights from Down syndromeTrafficking regulation of proteins in Alzheimer's diseaseMouse models of Down syndrome as a tool to unravel the causes of mental disabilitiesAmyloid β precursor protein as a molecular target for amyloid β--induced neuronal degeneration in Alzheimer's diseaseAlzheimer's disease therapeutics targeted to the control of amyloid precursor protein translation: maintenance of brain iron homeostasisNeurological phenotypes for Down syndrome across the life spanThe multifaceted nature of amyloid precursor protein and its proteolytic fragments: friends and foesDown Syndrome Cognitive Phenotypes Modeled in Mice Trisomic for All HSA 21 HomologuesGr33a modulates Drosophila male courtship preferenceDisruption of axonal transport perturbs bone morphogenetic protein (BMP)--signaling and contributes to synaptic abnormalities in two neurodegenerative diseasesNebula/DSCR1 upregulation delays neurodegeneration and protects against APP-induced axonal transport defects by restoring calcineurin and GSK-3β signalingPrincipal Component Analysis of the Effects of Environmental Enrichment and (-)-epigallocatechin-3-gallate on Age-Associated Learning Deficits in a Mouse Model of Down SyndromeSynaptic Vesicle Recycling Is Unaffected in the Ts65Dn Mouse Model of Down SyndromeInteractions between Aβ oligomers and presynaptic cholinergic signaling: age-dependent effects on attentional capacitiesAmyloid precursor protein-mediated endocytic pathway disruption induces axonal dysfunction and neurodegenerationAPP processing in Alzheimer's diseaseSynaptojanin 1-linked phosphoinositide dyshomeostasis and cognitive deficits in mouse models of Down's syndromeNovel 5' untranslated region directed blockers of iron-regulatory protein-1 dependent amyloid precursor protein translation: implications for down syndrome and Alzheimer's diseaseMonoacylglycerol lipase inhibitor JZL184 improves behavior and neural properties in Ts65Dn mice, a model of down syndromeAxonal transport and neurodegenerative disease: can we see the elephant?Neurodegenerative diseases target large-scale human brain networksProbing sporadic and familial Alzheimer's disease using induced pluripotent stem cellsPharmacological approaches to improving cognitive function in Down syndrome: current status and considerations.Comprehensive behavioral phenotyping of Ts65Dn mouse model of Down syndrome: activation of β1-adrenergic receptor by xamoterol as a potential cognitive enhancer.The use of mouse models to understand and improve cognitive deficits in Down syndrome.Brain plasticity and disease: a matter of inhibition.One at a time, live tracking of NGF axonal transport using quantum dotsThe amyloid-beta precursor protein is phosphorylated via distinct pathways during differentiation, mitosis, stress, and degeneration.Live imaging of neuronal connections by magnetic resonance: Robust transport in the hippocampal-septal memory circuit in a mouse model of Down syndrome.Amyloid precursor protein-induced axonopathies are independent of amyloid-beta peptides.
P2860
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P2860
Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年学术文章
@wuu
2006年学术文章
@zh-cn
2006年学术文章
@zh-hans
2006年学术文章
@zh-my
2006年学术文章
@zh-sg
2006年學術文章
@yue
2006年學術文章
@zh
2006年學術文章
@zh-hant
name
Increased App expression in a ...... olinergic neuron degeneration.
@en
Increased App expression in a ...... olinergic neuron degeneration.
@nl
type
label
Increased App expression in a ...... olinergic neuron degeneration.
@en
Increased App expression in a ...... olinergic neuron degeneration.
@nl
prefLabel
Increased App expression in a ...... olinergic neuron degeneration.
@en
Increased App expression in a ...... olinergic neuron degeneration.
@nl
P2093
P50
P1433
P1476
Increased App expression in a ...... holinergic neuron degeneration
@en
P2093
Angela Villar
Bruce T Lamb
Charles J Epstein
Chengbiao Wu
Gorazd B Stokin
Janice S Valletta
Jean-Dominique Delcroix
Laura Shapiro Kulnane
Lawrence S B Goldstein
P356
10.1016/J.NEURON.2006.05.022
P407
P577
2006-07-01T00:00:00Z