Journal Article

DZNE-2020-04069

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Effects of methylphenidate on the behavior of male 5xFAD mice.

Schneider, F. (First author)DZNE* ; Baldauf, K. (Corresponding author)DZNE* ; Wetzel, W. ; Reymann, K. (Last author)DZNE*

2015
Elsevier Science Amsterdam [u.a.]

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Please use a persistent id in citations: doi:10.1016/j.pbb.2014.11.006

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.

Keyword(s): Alzheimer Disease: drug therapy (MeSH) ; Alzheimer Disease: genetics (MeSH) ; Alzheimer Disease: psychology (MeSH) ; Amyloid beta-Protein Precursor: genetics (MeSH) ; Animals (MeSH) ; Anxiety: drug therapy (MeSH) ; Behavior, Animal: drug effects (MeSH) ; Behavior, Animal: physiology (MeSH) ; Central Nervous System Stimulants: pharmacology (MeSH) ; Disease Models, Animal (MeSH) ; Exploratory Behavior: drug effects (MeSH) ; Habituation, Psychophysiologic: drug effects (MeSH) ; Humans (MeSH) ; Male (MeSH) ; Maze Learning: drug effects (MeSH) ; Methylphenidate: pharmacology (MeSH) ; Mice (MeSH) ; Mice, Transgenic (MeSH) ; Motor Activity: drug effects (MeSH) ; Mutant Proteins: genetics (MeSH) ; Presenilin-1: genetics (MeSH) ; Amyloid beta-Protein Precursor ; Central Nervous System Stimulants ; Mutant Proteins ; PSEN1 protein, human ; Presenilin-1 ; Methylphenidate

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Contributing Institute(s):

1. Pathophysiology of Dementia (AG Reymann)
2. Core MR PET (Core MR PET)

Research Program(s):

1. 344 - Clinical and Health Care Research (POF3-344) (POF3-344)

Appears in the scientific report 2015

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Database coverage:
; BIOSIS Previews ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; Nationallizenz ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Web of Science Core Collection

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