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@ARTICLE{Schneider:137747,
author = {Schneider, F. and Baldauf, K. and Wetzel, W. and Reymann,
Klaus},
title = {{E}ffects of methylphenidate on the behavior of male
5x{FAD} mice.},
journal = {Pharmacology, biochemistry and behavior},
volume = {128},
issn = {0091-3057},
address = {Amsterdam [u.a.]},
publisher = {Elsevier Science},
reportid = {DZNE-2020-04069},
pages = {68-77},
year = {2015},
abstract = {Alzheimer's disease is a neurodegenerative disorder
characterized by a loss of memory and spatial orientation.
It is also reported that the dopamine system is affected.
Dopamine plays a prominent role in motor functions,
motivation, emotion, arousal and reward, and it is important
for learning and memory. One model that represents
characteristic hallmarks of Alzheimer's disease is the 5xFAD
mouse model, in which parenchymal plaque load starts at
2months of age. Transgenic 5xFAD mice show the first
behavioral deficits at 6months, which are evident at 9months
of age. In this study, we investigated the pharmacological
influence of methylphenidate (MPH) on behavioral deficits of
5xFAD mice. Using a battery of behavioral tests, we observed
no influence of MPH on anxiety in the elevated plus maze,
whereas the locomotion and explorative activity in the open
field was increased in transgenic and non-transgenic 5xFAD
mice after the application of MPH. Further MPH inhibits
habituation in the open field in healthy 5xFAD littermates
after the application of 10mg/kg MPH. On the other hand,
10mg/kg MPH improved spatial memory in 6-month-old
transgenic 5xFAD males, i.e., at a time point when deficits
start to occur. However, in 9-month-old transgenic mice, MPH
did not improve persisting learning and memory deficits. We
concluded that MPH might improve the non-cognitive,
apathy-like behavior (indicated by a reduced exploration),
but it has no influence on sustained Alzheimer typical
learning and memory deficits.},
keywords = {Alzheimer Disease: drug therapy / Alzheimer Disease:
genetics / Alzheimer Disease: psychology / Amyloid
beta-Protein Precursor: genetics / Animals / Anxiety: drug
therapy / Behavior, Animal: drug effects / Behavior, Animal:
physiology / Central Nervous System Stimulants: pharmacology
/ Disease Models, Animal / Exploratory Behavior: drug
effects / Habituation, Psychophysiologic: drug effects /
Humans / Male / Maze Learning: drug effects /
Methylphenidate: pharmacology / Mice / Mice, Transgenic /
Motor Activity: drug effects / Mutant Proteins: genetics /
Presenilin-1: genetics / Amyloid beta-Protein Precursor (NLM
Chemicals) / Central Nervous System Stimulants (NLM
Chemicals) / Mutant Proteins (NLM Chemicals) / PSEN1
protein, human (NLM Chemicals) / Presenilin-1 (NLM
Chemicals) / Methylphenidate (NLM Chemicals)},
cin = {AG Reymann / Core MR PET},
ddc = {540},
cid = {I:(DE-2719)1310005 / I:(DE-2719)1340016},
pnm = {344 - Clinical and Health Care Research (POF3-344)},
pid = {G:(DE-HGF)POF3-344},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:25449360},
doi = {10.1016/j.pbb.2014.11.006},
url = {https://pub.dzne.de/record/137747},
}