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: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype HPO
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 GeneticVariation phenotype BEFREE In two unrelated UK families with APP 717 val-ile mutations there was early prominent memory impairment with dyscalculia proceeding to generalized cognitive impairment with a lack of insight. 8239283 1993
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 GeneticVariation phenotype BEFREE Transgenic mice carrying AD-causing mutations in APP develop spontaneous age-related beta-amyloid (A beta) deposition and memory impairment. 9052714 1997
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype BEFREE Models of AD include: aged monkeys that show both cognitive/memory deficits and cellular abnormalities (amyloid deposition/cytoskeletal abnormalities of neurons) in cortex and hippocampus; and Tg mice that express mutant human FAD-linked genes (i.e., APP and PS1) and show increased levels of A.42, amyloid deposits, dystrophic neurites, and local responses of astrocytes and microglia. 9683997 1997
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 GeneticVariation phenotype BEFREE A recently described mouse line, Tg(HuAPP695.K670N/M671L)2576, expressing human amyloid precursor protein with a familial AD gene mutation, age-related amyloid deposits, and memory deficits, was found to develop a significant microglial response using Griffonia simplicifolia lectin or phosphotyrosine probe to identify microglia Both Griffonia simplicifolia lectin and phosphotyrosine staining showed increased numbers of intensely labeled, often enlarged microglia clustered in and around plaques, consistent with microglial activation related to beta-amyloid formation. 9422548 1998
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 GeneticVariation phenotype BEFREE We previously showed that mice over-expressing a human mutated form of APP (APP(V717F)) display age-dependent recognition memory deficits associated with the progression of amyloid deposition. 10718322 2000
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype BEFREE Although Abeta derived from the Abeta precursor protein (beta-APP) is believed to play a central etiological role in AD, it is not clear whether soluble and/or fibrillar forms are responsible for the memory deficit. 11724968 2001
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 AlteredExpression phenotype BEFREE Hippocampal A beta 42 levels correlate with spatial memory deficit in APP and PS1 double transgenic mice. 11950278 2002
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 GeneticVariation phenotype BEFREE Transgenic mice that overexpress the Swedish mutation of human amyloid precursor protein (hAPPswe; Tg2576) show age-dependent memory deficits in hippocampus-dependent learning tasks. 12359834 2002
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype BEFREE Thus far, the one manipulation found to mitigate the learning and memory deficits in APP transgenic mice is immunotherapy for A beta, either using active or passive immunization against the peptide. 12737527 2003
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype BEFREE The amyloid precursor protein + presenilin-1 (APP+PS1) transgenic mouse is a model for amyloid deposition, and like AD, the mice develop memory deficits as amyloid deposits accumulate. 12832546 2003
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 GeneticVariation phenotype BEFREE The Tg-APP (Sw, V717F)/B6 mice at 11-14 months displayed decreased motor coordination, learning and memory deficits, and severely increased anxiety. 15114629 2004
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 AlteredExpression phenotype BEFREE 129S6 mice are resistant to the lethal effects of APP overexpression, allowing sufficient levels of Abeta expression for the development of amyloid plaques and age-dependent memory deficits. 15254013 2004
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype CTD_human Beta-amyloid (1-42)-induced learning and memory deficits in mice: involvement of oxidative burdens in the hippocampus and cerebral cortex. 15364477 2004
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 GeneticVariation phenotype BEFREE Hypoxia treatment markedly increased Abeta deposition and neuritic plaque formation and potentiated the memory deficit in Swedish mutant APP transgenic mice. 17121991 2006
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 AlteredExpression phenotype BEFREE In conclusion, prolonged and localized APP695Swe expression in hippocampal neurons is sufficient to produce memory deficits without plaque formation or neuronal loss. 16780838 2006
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 GeneticVariation phenotype BEFREE BACE1 gene deletion prevents neuron loss and memory deficits in 5XFAD APP/PS1 transgenic mice. 17258906 2007
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype BEFREE In vivo treatment of London APP mice, expressing the WT beta-secretase site, with these inhibitors resulted in substantial improvement in memory deficit assessed by the Morris water maze test. 18184658 2008
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype CTD_human Release of acetylcholinesterase (AChE) from beta-amyloid plaques assemblies improves the spatial memory impairments in APP-transgenic mice. 18599028 2008
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype BEFREE Using aged ( approximately 16 months) amyloid precursor protein (APP) transgenic mice that exhibit increased production of the amyloid-beta (Abeta) peptide and severe cerebrovascular and memory deficits, we examined the capacity of in vivo treatments with the antioxidants N-acetyl-L-cysteine (NAC) and tempol, or the peroxisome proliferator-activated receptor gamma agonist pioglitazone to rescue cerebrovascular function and selected markers of AD neuropathology. 18784309 2008
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 AlteredExpression phenotype BEFREE Accumulations increased with age, and this was paralleled by decreased brain sizes on volumetric MRI, compared to age-matched and similar transgene-expressing APP wild-type mice, although, with these levels of transgenic expression we did not detect neuronal loss or significant memory impairment. 17112635 2008
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype BEFREE Previously, we reported that the stress associated with chronic isolation was associated with increased beta-amyloid (Abeta) plaque deposition and memory deficits in the Tg2576 transgenic animal model of Alzheimer's disease (AD) [Dong H, Goico B, Martin M, Csernansky CA, Bertchume A, Csernansky JG (2004) Effects of isolation stress on hippocampal neurogenesis, memory, and amyloid plaque deposition in APP (Tg2576) mutant mice.Neuroscience 127:601-609]. 18571864 2008
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype CTD_human Adenosine A2A receptor blockade prevents memory dysfunction caused by beta-amyloid peptides but not by scopolamine or MK-801. 18191838 2008
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype BEFREE Increase in presenilin 1 (PS1) levels in senescence-accelerated mice (SAMP8) may indirectly impair memory by affecting amyloid precursor protein (APP) processing. 19181896 2009
CUI: C0233794
Disease: Memory impairment
Memory impairment
0.500 Biomarker phenotype CTD_human Evaluation of the protective role of melatonin on the behavioral effects of aluminum in a mouse model of Alzheimer's disease. 19770021 2009