| protein
| gamma secretase putatively (PSEN1 and PSEN2) to cleavage of APP in Abeta 42 with deposition in brain (fibrillar myeloid plaques to cause neurodegeneration) |
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APBB1, via its C-ter region (LRP2 interacts with APP and APBB1 in neurons  |
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sortilin-related receptor, L(DLR class) A repeats-containing (SORL1) |
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APP and APLP bind to heme oxygenase (HO) and inhibit HO activity |
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amyloid beta (A4) precursor protein-binding, family B, member 1 (Fe65) |
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forms a multimeric complex with the nuclear adaptor protein Fe65 and the histone acetyltransferase Tip60 |
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amyloid beta (A4) precursor protein-binding, family A, member 1 (APBA1) |
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amyloid beta (A4) precursor protein-binding, family A, member 2 (ABPA2) |
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amyloid beta (A4) precursor protein-binding, family A, member 3 (APBA3) |
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amyloid beta (A4) precursor protein-binding, family B, member 2 (APBB2) |
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amyloid beta (A4) precursor protein-binding, family B, member 3 (APBB3) |
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acetylcholinesterase (AChE) |
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protein interacting with APP tail 1 (PAT1) |
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heparan sulfate proteoglycan 2 (HSPG2) |
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Human bleomycin hydrolase (hBH) |
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Disruption of the disabled-1 gene (Dab1) |
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fibulin 1 (FBLN1) |
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Calreticulin (CALR) |
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glyceraldehyde-3-phosphate dehydrogenase (GAPDH) |
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growth factor receptor-bound protein 2 (GRB2) |
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SHC (Src homology 2 domain containing) transforming protein 1 (SHC1) |
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gelsolin (GSN) |
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intracellular amyloid beta-peptide (A beta) binding protein (ERAB) |
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kinesin-I |
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kininogen 1 (KING1) |
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low density lipoprotein (LDL) receptor-related protein 1B (LRP1B) |
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Jun NH2-terminal kinase (JNK) interacting protein 1 (JIP1) |
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59-kDa APP-binding protein, called APP-BP1 |
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nicastrin (NCSTN) |
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Notch inhibitors Numb and Numb-like in mouse brain |
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alpha 1-antichymotrypsin (ACT) |
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synuclein, alpha (non A4 component of amyloid precursor) (SNCA) |
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spondin 1, extracellular matrix protein (SPON1) |
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Transforming growth factor-beta (TGF-beta) |
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TM2 domain containing 1 (TM2D1) |
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mitogen-activated protein kinase 8 interacting protein 1 (MAPK8IP1 aslo known as JIP-1) |
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presenilin 1 (PS1) and presenilin 2 (PS2) |
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human serine protease HtrA2/Omi |
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death receptor 6 (DR6) |
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alpha7 nicotinic acetylcholine receptor (alpha7nAChR) |
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cell death mediator p75(NTR) |
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microtubule-associated protein tau (MAPT) |
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have major interactions with ferroportin to facilitate iron export from certain cells including neurons |
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GAS1 negatively regulated APP intracellular trafficking |
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GULP1-APP interaction is mediated by the NPTY motif of APP and the GULP1 PTB (phosphotyrosine-binding) domain ( |
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CDH2 expression facilitates cis-dimerization of APP ( |
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interaction between APP and neuroligin-1 (NLGN1), increasing the formation of APP oligomers, and suggesting that this interaction could triggers the targeting of APP oligomer to the postsynaptic regions of excitatory synapses |
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| transgenic mouse models expressing human Alzheimer's A beta peptide exhibit brain regions severely affected in Alzheimer's disease resulting in extensive neuronal degeneration (LaFerla 1995) | |
double mutant (tau/APP) mice exhibited neurofibrillary tangle pathology substantially enhanced in the limbic system and olfactory cortex (Lewis 2001) |
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co-expression of both mutant transgenes presenilin 1 and APP results in acceleration of amyloid accumulation and associative learning deficits (Dineley 2002) |
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expression of human Abeta42 peptide in the Drosophila brain led to the formation of diffused amyloid deposits, age-dependent learning defects, and extensive neurodegeneration and Abeta40 caused only age-dependent learning defects (Iijima 2004) |
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FVB/N mice overexpressing human APP695 develop a central nervous system disorder and die prematurely, precluding development of Abeta peptide amyloid plaques whereas 129S6 mice are resistant to the lethal effects of APP overexpression (Krezowski 2004) |
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gene expression analysis revealed that the genes related to mitochondrial energy metabolism and apoptosis were up-regulated in 2-month-old Tg2576 mouse AD model and that the same genes were up-regulated at 5 and 18 months of age suggesting that mitochondrial energy metabolism is impaired by the expression of mutant APP and/or Abeta, and that the up-regulation of mitochondrial genes is a compensatory response (Reddy 2004) |
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estrogen-deficient APP23 mice exhibited greatly reduced brain estrogen, early-onset and increased beta amyloid peptide (Abeta) deposition and increased Abeta production (Yue 2005) |
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memory deficits in middle-aged Tg2576 mice are caused by the extracellular accumulation of a 56-kDa soluble amyloid-beta assembly suggesting that Abeta*56 impairs memory independently of plaques or neuronal loss, and may contribute to cognitive deficits associated with Alzheimer's disease (Lesné 2006) |
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Lack of NO synthase 2 in the amyloid precursor protein Swedish mutant mouse increased insoluble beta-amyloid peptide levels, neuronal degeneration, caspase-3 activation, and tau cleavage (Colton 2006) |
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Alzheimer disease mice deficient in Ccr2 accumulated Abeta earlier and died prematurely. Ccr2 deficiency accelerates early disease progression and markedly impairs microglial accumulation (El Khoury 2007) |
