APP, amyloid beta precursor protein, 351

N. diseases: 485; N. variants: 114
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE M344 also increases levels of immature APP, supporting an effect on APP trafficking, concurrent with the observed increase in MINT2 and FE65, both shown to increase immature APP in the early secretory pathway.Chronic i.p. treatment of the triple transgenic (APP<sub>sw</sub>/PS1<sub>M146V</sub>/Tau<sub>P301L</sub>) mice with M344, at doses as low as 3 mg/kg, significantly prevented cognitive decline evaluated by Y-maze spontaneous alternation, novel object recognition, and Barnes maze spatial memory tests. 29073110 2017
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE The high accumulation of the CB-RBCMs in neurons resulted in a decrease in the neurotoxicity of CB and an increase in the migratory activity of neurons, and alleviated cognitive decline in APP/PS1 transgenic (Tg) mice. 28865290 2017
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE MT5-MMP emerges as a new pro-amyloidogenic regulator of APP metabolism, whose deficiency alleviates amyloid pathology, neuroinflammation and cognitive decline. 26202697 2016
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE To further explore how MgT treatment inhibits cognitive decline in APP/PS1 Tg mice, the critical molecules for amyloid precursor protein (APP) cleavage and signaling pathways were investigated. 26293690 2015
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype CTD_human Exposure to As-, Cd-, and Pb-mixture induces Aβ, amyloidogenic APP processing and cognitive impairments via oxidative stress-dependent neuroinflammation in young rats. 25288670 2015
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 AlteredExpression phenotype BEFREE In this study, we investigated the effect of T4 on cognitive decline and synaptic plasticity in five times familial AD (5XFAD) mice co-expressing mutated amyloid precursor protein and presenilin-1. 25661995 2015
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE However, the most widely used transgenic AD models (overexpressing mutated forms of amyloid precursor protein, presenilin, and/or tau) do not demonstrate the degree of inflammation, neurodegeneration (particularly of the cholinergic system), and cognitive decline that is comparable with the human disease. 25025046 2014
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 GeneticVariation phenotype BEFREE We report a novel missense mutation, D678H, in the APP gene in a Taiwanese patient who had progressive cognitive decline beginning in middle age. 23931937 2014
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE The studied dendrimers did not reverse memory impairment in APP/PS1 mice following chronic administration; moreover, cationic G4mOS caused cognitive decline in nontransgenic mice. 24004423 2013
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 GeneticVariation phenotype BEFREE We found a coding mutation (A673T) in the APP gene that protects against Alzheimer's disease and cognitive decline in the elderly without Alzheimer's disease. 22801501 2012
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 GeneticVariation phenotype BEFREE We found a novel APP mutation (A673V) in the homozygous state in a patient with early-onset AD-type dementia and in his younger sister showing initial signs of cognitive decline. 22727994 2012
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 AlteredExpression phenotype BEFREE The results suggest interaction between chronic cerebral hypoperfusion and APP(Sw/Ind) overexpression in cognitive decline in mice through enhanced neuronal loss and altered amyloid β metabolism. 21305033 2011
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE Progressive neuropathology and cognitive decline in a single Arctic APP transgenic mouse model. 19329229 2011
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE These results offer additional support for the negative impact of apoE4 on both memory and attention and further suggest that APP-Yac/apoE-TR mice provide a novel and useful model for investigating the role of apoE in mediating susceptibility to cognitive decline. 20002203 2010
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE The findings unveil a previously unrecognized role of Nox2-derived radicals in the behavioral deficits of Tg2576 mice and provide a link between the neurovascular dysfunction and cognitive decline associated with amyloid pathology. 18202172 2008
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 AlteredExpression phenotype BEFREE Thus, changes in APP and tau expression may cause perturbed axonal transport and changes in APP processing, contributing to cognitive decline and neurodegeneration in Alzheimer's disease. 17047360 2006
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 AlteredExpression phenotype BEFREE Interleukin-6 (IL-6), an inflammatory cytokine, is thought to play a role in neurodegeneration of the central nervous system and has been associated with increased amyloid precursor protein expression in vitro and greater cognitive decline. 15193763 2004
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE We hypothesize that the functional loss of members of the APP family contributes to the gradual cognitive decline in Alzheimer's disease patients. 10578233 1999
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 Biomarker phenotype BEFREE Genetic variability at APOE and APP was not significantly associated with evidence of cognitive decline. 9189907 1997
CUI: C0234985
Disease: Mental deterioration
Mental deterioration
0.400 GeneticVariation phenotype BEFREE Since interleukin-1 (IL-1) is an APP gene promoter showing a progressive increase in body fluids in parallel with mental deterioration in AD patients, we have studied the effects of CDP-choline on cognition, several biological parameters, and IL-1 beta production in AD and multi-infarct dementia (MID) in order to elucidate whether this compound alone or in combination with other drugs is able to restore immune function and improve mental performance in senile dementia. 8239305 1993