title: APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD).
abstract: The discovery of gene mutations responsible for autosomal dominant Alzheimer's disease has enabled researchers to reproduce in transgenic mice several hallmarks of this disorder, notably Aβ accumulation, though in most cases without neurofibrillary tangles. Mice expressing mutated and wild-type APP as well as C-terminal fragments of APP exhibit variations in exploratory activity reminiscent of behavioural and psychological symptoms of Alzheimer dementia (BPSD). In particular, open-field, spontaneous alternation, and elevated plus-maze tasks as well as aggression are modified in several APP transgenic mice relative to non-transgenic controls. However, depending on the precise murine models, changes in open-field and elevated plus-maze exploration occur in either direction, either increased or decreased relative to controls. It remains to be determined which neurotransmitter changes are responsible for this variability, in particular with respect to GABA, 5HT, and dopamine.
authors.affiliation: Département de Psychologie, Faculté des Sciences, Université de Rouen, 76821 Mont-Saint-Aignan Cedex, France. robert.lalonde@univ-rouen.fr
authors.forename: R
authors.initials: R
authors.lastname: Lalonde
authors.forename: K
authors.initials: K
authors.lastname: Fukuchi
authors.forename: C
authors.initials: C
authors.lastname: Strazielle
mesh_terms: D016564:Amyloid beta-Protein Precursor / Q000235:genetics*; D000818:Animals; D001526:Behavioral Symptoms / Q000235:genetics* / Q000523:psychology*; D003704:Dementia / Q000235:genetics* / Q000523:psychology*; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D009154:Mutation
chemical_list: D016564:Amyloid beta-Protein Precursor