Reversal of learning deficits in hAPP transgenic mice carrying a mutation at Asp664: a role for early experience - Wikidata - wikimedia - TriplyDB

Reversal of learning deficits in hAPP transgenic mice carrying a mutation at Asp664: a role for early experience

Reversal of learning deficits in hAPP transgenic mice carrying a mutation at Asp664: a role for early experience

http://www.wikidata.org/entity/Q42110206

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Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease Amyloid β precursor protein as a molecular target for amyloid β--induced neuronal degeneration in Alzheimer's disease Many neuronal and behavioral impairments in transgenic mouse models of Alzheimer's disease are independent of caspase cleavage of the amyloid precursor protein Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice.Chronic rapamycin restores brain vascular integrity and function through NO synthase activation and improves memory in symptomatic mice modeling Alzheimer's disease.Cleavage at the 586 amino acid caspase-6 site in mutant huntingtin influences caspase-6 activation in vivo.Chronic inhibition of mammalian target of rapamycin by rapamycin modulates cognitive and non-cognitive components of behavior throughout lifespan in mice Importance of the caspase cleavage site in amyloid-β protein precursor Caspase-6 as a novel early target in the treatment of Alzheimer's disease.The amyloid precursor protein intracellular domain-fe65 multiprotein complexes: a challenge to the amyloid hypothesis for Alzheimer's disease?Palmitoylation of caspase-6 by HIP14 regulates its activation.Over-expression of heat shock factor 1 phenocopies the effect of chronic inhibition of TOR by rapamycin and is sufficient to ameliorate Alzheimer's-like deficits in mice modeling the disease.

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Reversal of learning deficits in hAPP transgenic mice carrying a mutation at Asp664: a role for early experience

http://www.wikidata.org/entity/Q42110206

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2009 nî lūn-bûn

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Reversal of learning deficits ...... 4: a role for early experience

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Reversal of learning deficits ...... 4: a role for early experience

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Reversal of learning deficits ...... 4: a role for early experience

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Reversal of learning deficits ...... 4: a role for early experience

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J.BBR.2009.09.013

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Behavioural Brain Research

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Reversal of learning deficits ...... 4: a role for early experience

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Dale E Bredesen

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Huidong Tang

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Junli Zhang

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Olivia F Gorostiza

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Veronica Galvan

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P2860

c-Jun N-terminal kinase (JNK)-interacting protein-1b/islet-brain-1 scaffolds Alzheimer's amyloid precursor protein with JNK

Homo- and heterodimerization of APP family members promotes intercellular adhesion.

Axonal transport of amyloid precursor protein is mediated by direct binding to the kinesin light chain subunit of kinesin-I

Disabled-1 binds to the cytoplasmic domain of amyloid precursor-like protein 1

Involvement of caspases in proteolytic cleavage of Alzheimer's amyloid-beta precursor protein and amyloidogenic A beta peptide formation

Synergistic effects of Munc18a and X11 proteins on amyloid precursor protein metabolism

Cell biology of the amyloid beta-protein precursor and the mechanism of Alzheimer's disease

The intracellular domain of the beta-amyloid precursor protein is stabilized by Fe65 and translocates to the nucleus in a notch-like manner

High-level neuronal expression of abeta 1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation

Developments of a water-maze procedure for studying spatial learning in the rat

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10.1016/J.BBR.2009.09.013

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