Enhanced amyloidogenic processing of the beta-amyloid precursor protein in gene-targeted mice bearing the Swedish familial Alzheimer's disease mutations and a "humanized" Abeta sequence.
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Gavage of D-Ribose induces Aβ-like deposits, Tau hyperphosphorylation as well as memory loss and anxiety-like behavior in miceCaveolae, plasma membrane microdomains for alpha-secretase-mediated processing of the amyloid precursor proteinModeling Alzheimer's disease in mouse without mutant protein overexpression: cooperative and independent effects of Aβ and tauCerebral blood flow changes after brain injury in human amyloid-beta knock-in miceShort-term treatment with tolfenamic acid improves cognitive functions in Alzheimer's disease miceAge-related loss of phospholipid asymmetry in APP(NLh)/APP(NLh) x PS-1(P264L)/PS-1(P264L) human double mutant knock-in mice: relevance to Alzheimer disease.APP transgenic modeling of Alzheimer's disease: mechanisms of neurodegeneration and aberrant neurogenesisHumanized SFTPA1 and SFTPA2 transgenic mice reveal functional divergence of SP-A1 and SP-A2: formation of tubular myelin in vivo requires both gene productsAnimal models of amyloid-beta-related pathologies in Alzheimer's disease.Gene-environment interaction research and transgenic mouse models of Alzheimer's disease.Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficitsObesity and diabetes cause cognitive dysfunction in the absence of accelerated β-amyloid deposition in a novel murine model of mixed or vascular dementia.Combination therapy prevents amyloid-dependent and -independent structural changes.Beta-amyloid mediated nitration of manganese superoxide dismutase: implication for oxidative stress in a APPNLH/NLH X PS-1P264L/P264L double knock-in mouse model of Alzheimer's disease.Long-term accumulation of amyloid-beta, beta-secretase, presenilin-1, and caspase-3 in damaged axons following brain traumaAtherosclerosis and Alzheimer--diseases with a common cause? Inflammation, oxysterols, vasculatureClosed head injury in an age-related Alzheimer mouse model leads to an altered neuroinflammatory response and persistent cognitive impairment.Long-lasting impairment in hippocampal neurogenesis associated with amyloid deposition in a knock-in mouse model of familial Alzheimer's disease.Amyloid deposition and advanced age fails to induce Alzheimer's type progression in a double knock-in mouse modelDecreased brain-derived neurotrophic factor depends on amyloid aggregation state in transgenic mouse models of Alzheimer's disease.Recent advances in transgenic model development for Alzheimer's disease.Enhanced β-secretase processing alters APP axonal transport and leads to axonal defects.Unusual phenotypic alteration of beta amyloid precursor protein (betaAPP) maturation by a new Val-715 --> Met betaAPP-770 mutation responsible for probable early-onset Alzheimer's disease.Sex and gonadal hormones in mouse models of Alzheimer's disease: what is relevant to the human condition?A neuronal model of Alzheimer's disease: an insight into the mechanisms of oxidative stress-mediated mitochondrial injury.Transgenic models of Alzheimer's disease: better utilization of existing models through viral transgenesis.Context dependent function of APPb enhancer identified using enhancer trap-containing BACs as transgenes in zebrafish.Comprehensive behavioral characterization of an APP/PS-1 double knock-in mouse model of Alzheimer's diseaseDifferential transgene expression patterns in Alzheimer mouse models revealed by novel human amyloid precursor protein-specific antibodiesTs1Cje, a partial trisomy 16 mouse model for Down syndrome, exhibits learning and behavioral abnormalities.APP transgenic mice: their use and limitations.APP physiological and pathophysiological functions: insights from animal models.Mouse models of Alzheimer's disease.Modeling human neurodegenerative diseases in transgenic systems.Alzheimer's disease in the retina: imaging retinal aβ plaques for early diagnosis and therapy assessment.Retinal manifestations of Alzheimer's disease.Cognitive impairment in humanized APP×PS1 mice is linked to Aβ(1-42) and NOX activation.Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic miceProteomic identification of specifically carbonylated brain proteins in APP(NLh)/APP(NLh) × PS-1(P264L)/PS-1(P264L) human double mutant knock-in mice model of Alzheimer disease as a function of ageCystatin C protects neuronal cells from amyloid-beta-induced toxicity.
P2860
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P2860
Enhanced amyloidogenic processing of the beta-amyloid precursor protein in gene-targeted mice bearing the Swedish familial Alzheimer's disease mutations and a "humanized" Abeta sequence.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年学术文章
@wuu
1996年学术文章
@zh
1996年学术文章
@zh-cn
1996年学术文章
@zh-hans
1996年学术文章
@zh-my
1996年学术文章
@zh-sg
1996年學術文章
@yue
1996年學術文章
@zh-hant
name
Enhanced amyloidogenic process ...... a "humanized" Abeta sequence.
@en
Enhanced amyloidogenic process ...... a "humanized" Abeta sequence.
@nl
type
label
Enhanced amyloidogenic process ...... a "humanized" Abeta sequence.
@en
Enhanced amyloidogenic process ...... a "humanized" Abeta sequence.
@nl
prefLabel
Enhanced amyloidogenic process ...... a "humanized" Abeta sequence.
@en
Enhanced amyloidogenic process ...... a "humanized" Abeta sequence.
@nl
P2093
P2860
P356
P1476
Enhanced amyloidogenic process ...... a "humanized" Abeta sequence.
@en
P2093
Greenberg BD
Howland DS
P2860
P304
23380-23388
P356
10.1074/JBC.271.38.23380
P407
P577
1996-09-01T00:00:00Z