Neprilysin overexpression inhibits plaque formation but fails to reduce pathogenic Abeta oligomers and associated cognitive deficits in human amyloid precursor protein transgenic mice.
about
Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's diseaseThe neurotrophic compound J147 reverses cognitive impairment in aged Alzheimer's disease miceNeuregulin 1 improves cognitive deficits and neuropathology in an Alzheimer's disease model.Intracellular cleavage of amyloid β by a viral protease NIa prevents amyloid β-mediated cytotoxicityPeripheral delivery of a CNS targeted, metalo-protease reduces aβ toxicity in a mouse model of Alzheimer's diseaseStem cells in human neurodegenerative disorders--time for clinical translation?2-Deoxy-D-glucose treatment induces ketogenesis, sustains mitochondrial function, and reduces pathology in female mouse model of Alzheimer's diseaseChronic Anatabine Treatment Reduces Alzheimer's Disease (AD)-Like Pathology and Improves Socio-Behavioral Deficits in a Transgenic Mouse Model of ADEnvironmental enrichment strengthens corticocortical interactions and reduces amyloid-β oligomers in aged mice.Transsynaptic progression of amyloid-β-induced neuronal dysfunction within the entorhinal-hippocampal network.Many neuronal and behavioral impairments in transgenic mouse models of Alzheimer's disease are independent of caspase cleavage of the amyloid precursor proteinA coimmunization vaccine of Aβ42 ameliorates cognitive deficits without brain inflammation in an Alzheimer's disease model.FcγRIIb mediates amyloid-β neurotoxicity and memory impairment in Alzheimer's disease.Biochemical and immunohistochemical analysis of an Alzheimer's disease mouse model reveals the presence of multiple cerebral Abeta assembly forms throughout life.Neural stem cells genetically-modified to express neprilysin reduce pathology in Alzheimer transgenic modelsThe nuclear inclusion a (NIa) protease of turnip mosaic virus (TuMV) cleaves amyloid-βA neuroprotective brain-penetrating endopeptidase fusion protein ameliorates Alzheimer disease pathology and restores neurogenesis.Effect of rosiglitazone on amyloid precursor protein processing and Aβ clearance in streptozotocin-induced rat model of Alzheimer's disease.A novel Alzheimer's disease drug candidate targeting inflammation and fatty acid metabolism.Distinctive RNA expression profiles in blood associated with Alzheimer disease after accounting for white matter hyperintensities.Circulating neprilysin clears brain amyloidPathological Hallmarks, Clinical Parallels, and Value for Drug Testing in Alzheimer's Disease of the APP[V717I] London Transgenic Mouse Model.Expression and functional profiling of neprilysin, insulin-degrading enzyme, and endothelin-converting enzyme in prospectively studied elderly and Alzheimer's brain.New therapeutic approaches for Alzheimer's disease and cerebral amyloid angiopathy.C-terminal-truncated apolipoprotein (apo) E4 inefficiently clears amyloid-beta (Abeta) and acts in concert with Abeta to elicit neuronal and behavioral deficits in mice.Neuroinflammation and neuronal loss precede Aβ plaque deposition in the hAPP-J20 mouse model of Alzheimer's disease.Neprilysin-2 is an important β-amyloid degrading enzyme.HIV-1 Tat interacts with and regulates the localization and processing of amyloid precursor protein.A combination Alzheimer's therapy targeting BACE1 and neprilysin in 5XFAD transgenic mice.Soluble Aβ oligomer production and toxicity.Ablation of cellular prion protein does not ameliorate abnormal neural network activity or cognitive dysfunction in the J20 line of human amyloid precursor protein transgenic mice.Somatostatin receptor subtype-4 agonist NNC 26-9100 decreases extracellular and intracellular Aβ₁₋₄₂ trimers.Targeting protein aggregation for the treatment of degenerative diseasesExogenous expression of Drp1 plays neuroprotective roles in the Alzheimer's disease in the Aβ42 transgenic Drosophila model.Safety of the neprilysin/renin-angiotensin system inhibitor LCZ696.Advances in the pathogenesis of Alzheimer's disease: a re-evaluation of amyloid cascade hypothesis.Increasing the Receptor Tyrosine Kinase EphB2 Prevents Amyloid-β-induced Depletion of Cell Surface Glutamate Receptors by a Mechanism That Requires the PDZ-binding Motif of EphB2 and Neuronal Activity.Expression of the plant viral protease NIa in the brain of a mouse model of Alzheimer's disease mitigates Aβ pathology and improves cognitive functionInsulin receptor signaling mediates APP processing and β-amyloid accumulation without altering survival in a transgenic mouse model of Alzheimer's diseaseThe complex PrP(c)-Fyn couples human oligomeric Aβ with pathological tau changes in Alzheimer's disease.
P2860
Q21136406-AE4A6507-2E6D-40A9-A85F-3CA32F540C7BQ21195685-B6804F1A-12B1-404E-9588-5C1A7ED85033Q27316651-FC19AF61-CB63-4608-8987-F80BDCF96C01Q27324934-B661B8C8-AD3F-48C1-AA64-F812568506B8Q27437619-365F2E97-446F-407C-B3C5-237C7DBBCB72Q27687068-27B25E82-7C71-4BC7-9C3D-2BB98732A867Q28478912-6176C472-45F4-4526-A5E8-F896C8246B54Q28547449-23C59C78-74AD-42B6-B192-6222B535FC4EQ30443842-929EA31C-0449-4AB5-8AC4-F60CB4B3A90DQ30498362-375E8347-21D0-43DC-BCA0-E78D99D280CDQ30499149-60F757BD-1E89-49F7-98F0-F6C262726BB2Q30581976-6D99B071-DEEF-4DF4-9A01-505AC6BB8760Q30664429-69C54684-2E20-43CA-BBB6-B8CD1C08A55BQ33292558-53CF56BA-0905-470D-93A4-6595AC4E2893Q33746410-F3A82BA9-E419-47AE-89B7-01280EBC7962Q33781167-8141DF7D-9F90-4659-BB6D-059E78BACABCQ33793059-0EACCE54-A2D2-4F44-86E6-F7B8B603A747Q33819563-69280EFF-B22C-4FFC-B5A7-BDE36BA8B6CCQ33909566-2FA5904D-11B6-493F-A906-9841C1A673F1Q34071221-052AB19D-A102-420A-933C-06AD58611FA2Q34071954-254428EC-9376-4408-B23C-544FA6416A4CQ34127547-C04D760A-CF75-4D0D-9F25-C392E23960D3Q34130147-9C259782-2048-4060-BEF7-70C516823DF7Q34368970-BF817D23-6D9F-4BCB-B62D-979E498281AEQ34651878-794CE77C-8CA9-47FC-A10B-9D2F99DE2837Q34656208-C5F970F8-2621-460B-AC05-C41157973FCFQ34755720-4D8AA6A2-8D33-42FA-9028-6A3DA8E186B6Q35060145-749CEF6B-8D1C-4AF1-AA84-E8609899E488Q35426661-65322A05-D3AD-4359-99BD-39F85C4CC4CFQ35663419-214A91A7-D324-47C1-B1BC-27199C4A98A0Q35856815-1D2C385D-5338-40EA-936E-8A71EFD031A3Q35923336-ED8B65AA-BA34-4729-ABCA-E795D575B3ADQ36235980-D805DDB6-3D95-4FDF-9948-8064A6795DF4Q36377666-4D2FD511-66B4-4048-877A-DD77F4B3F257Q36405279-B32494A7-86B1-4242-BDA8-4E9B09C78C7BQ36478423-3AA47AAF-8E6A-45A7-A062-D897EFD11554Q36489274-B9155C2D-5DC5-4487-958A-B2305B407574Q36514449-7291FCD9-C2C9-4677-BD1A-4F959FB4E131Q36528274-E77E2F7B-ACB2-4551-B0E0-99364702216EQ36600160-DC7FDA40-3E82-48A5-8618-612CB9AA6FF0
P2860
Neprilysin overexpression inhibits plaque formation but fails to reduce pathogenic Abeta oligomers and associated cognitive deficits in human amyloid precursor protein transgenic mice.
description
2009 nî lūn-bûn
@nan
2009 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
name
Neprilysin overexpression inhi ...... ursor protein transgenic mice.
@ast
Neprilysin overexpression inhi ...... ursor protein transgenic mice.
@en
type
label
Neprilysin overexpression inhi ...... ursor protein transgenic mice.
@ast
Neprilysin overexpression inhi ...... ursor protein transgenic mice.
@en
prefLabel
Neprilysin overexpression inhi ...... ursor protein transgenic mice.
@ast
Neprilysin overexpression inhi ...... ursor protein transgenic mice.
@en
P2093
P2860
P1476
Neprilysin overexpression inhi ...... ursor protein transgenic mice.
@en
P2093
Gui-Qiu Yu
Irene H Cheng
Kaitlyn Ho
Kimberly Scearce-Levie
Lennart Mucke
Luke A Esposito
Moustapha Cisse
Tiffany Wu
William J Meilandt
P2860
P304
P356
10.1523/JNEUROSCI.2984-08.2009
P407
P577
2009-02-01T00:00:00Z