Alzheimer's disease-like pathological features in transgenic mice expressing the APP intracellular domain. - Wikidata - wikimedia - TriplyDB

Alzheimer's disease-like pathological features in transgenic mice expressing the APP intracellular domain.

Alzheimer's disease-like pathological features in transgenic mice expressing the APP intracellular domain.

http://www.wikidata.org/entity/Q37389332

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Alzheimer mechanisms and therapeutic strategies Synapses and Alzheimer's disease Fundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's disease in focal cerebral ischemic rats Fundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's disease Clinical proteomics of enervated neurons Alzheimer's Disease: Mechanism and Approach to Cell Therapy Parallels between major depressive disorder and Alzheimer's disease: role of oxidative stress and genetic vulnerability Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer's disease Alzheimer's disease, amyloid peptide and synaptic dysfunction The multifaceted nature of amyloid precursor protein and its proteolytic fragments: friends and foes Abnormal cognition, sleep, EEG and brain metabolism in a novel knock-in Alzheimer mouse, PLB1 APP intracellular domain impairs adult neurogenesis in transgenic mice by inducing neuroinflammation Tau Protein Mediates APP Intracellular Domain (AICD)-Induced Alzheimer's-Like Pathological Features in Mice Stem Cell Therapy: A Prospective Treatment for Alzheimer's Disease Proteolytic processing of Alzheimer's β-amyloid precursor protein The Ubiquitin-Proteasome System and Molecular Chaperone Deregulation in Alzheimer's Disease Transgenic expression of the amyloid-beta precursor protein-intracellular domain does not induce Alzheimer's Disease-like traits in vivo Interaction of Grb2 SH3 domain with UVRAG in an Alzheimer's disease-like scenario.Oral Triphenylmethane Food Dye Analog, Brilliant Blue G, Prevents Neuronal Loss in APPSwDI/NOS2-/- Mouse Model.The Psen1-L166P-knock-in mutation leads to amyloid deposition in human wild-type amyloid precursor protein YAC transgenic mice.Transsynaptic progression of amyloid-β-induced neuronal dysfunction within the entorhinal-hippocampal network.APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant Hirano bodies differentially modulate cell death induced by tau and the amyloid precursor protein intracellular domain.Abnormal neuronal networks and seizure susceptibility in mice overexpressing the APP intracellular domain.Cellular levels of Grb2 and cytoskeleton stability are correlated in a neurodegenerative scenario.An overview of APP processing enzymes and products.Knock-in of human BACE1 cleaves murine APP and reiterates Alzheimer-like phenotypes The role of tau kinases in Alzheimer's disease.Knockdown of amyloid precursor protein in zebrafish causes defects in motor axon outgrowth.When neurogenesis encounters aging and disease Model Hirano bodies protect against tau-independent and tau-dependent cell death initiated by the amyloid precursor protein intracellular domain.Novel adaptors of amyloid precursor protein intracellular domain and their functional implications.The β-secretase-derived C-terminal fragment of βAPP, C99, but not Aβ, is a key contributor to early intraneuronal lesions in triple-transgenic mouse hippocampus.Targets for AD treatment: conflicting messages from γ-secretase inhibitors Turnover of amyloid precursor protein family members determines their nuclear signaling capability GSK-3 in Neurodegenerative Diseases.Amyloid beta-mediated cell death of cultured hippocampal neurons reveals extensive Tau fragmentation without increased full-length tau phosphorylation.The roles of amyloid precursor protein (APP) in neurogenesis: Implications to pathogenesis and therapy of Alzheimer disease.Biochemical inhibition of the acetyltransferases ATase1 and ATase2 reduces β-secretase (BACE1) levels and Aβ generation Biochemical and morphological characterization of the AβPP/PS/tau triple transgenic mouse model and its relevance to sporadic Alzheimer's disease.

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P2860

Alzheimer's disease-like pathological features in transgenic mice expressing the APP intracellular domain.

http://www.wikidata.org/entity/Q37389332

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 16 October 2009

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Alzheimer's disease-like patho ...... the APP intracellular domain.

@en

Alzheimer's disease-like patho ...... the APP intracellular domain.

@nl

type

label

Alzheimer's disease-like patho ...... the APP intracellular domain.

@en

Alzheimer's disease-like patho ...... the APP intracellular domain.

@nl

prefLabel

Alzheimer's disease-like patho ...... the APP intracellular domain.

@en

Alzheimer's disease-like patho ...... the APP intracellular domain.

@nl

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PNAS.0907652106

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Proceedings of the National Academy of Sciences of the United States of America

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Alzheimer's disease-like patho ...... g the APP intracellular domain

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Bruce T Lamb

http://www.w3.org/2001/XMLSchema#string

Kaushik Ghosal

http://www.w3.org/2001/XMLSchema#string

Man Liang

http://www.w3.org/2001/XMLSchema#string

Sanjay W Pimplikar

http://www.w3.org/2001/XMLSchema#string

Yong Shen

http://www.w3.org/2001/XMLSchema#string

P2860

The gamma -secretase-cleaved C-terminal fragment of amyloid precursor protein mediates signaling to the nucleus

Amyloid precursor protein regulates brain apolipoprotein E and cholesterol metabolism through lipoprotein receptor LRP1

Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer's disease

The amyloid precursor protein: beyond amyloid

The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide

A transcriptionally [correction of transcriptively] active complex of APP with Fe65 and histone acetyltransferase Tip60

Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein

The ubiquitin-proteasome system in Alzheimer's disease

A specific amyloid-beta protein assembly in the brain impairs memory

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scholarly article

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19837693

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Alzheimer's disease

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2762847

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