TY - JOUR
T1 - Effects of pharmacological agents, sleep deprivation, hypoxia and transcranial magnetic stimulation on electroencephalographic rhythms in rodents: towards translational challenge models for drug discovery in Alzheimer's disease
AU - Babiloni, Claudio
AU - Infarinato, Francesco
AU - Aujard, Fabienne
AU - Bastlund, Jesper Frank
AU - Bentivoglio, Marina
AU - Bertini, Giuseppe
AU - Del Percio, Claudio
AU - Fabene, Paolo Francesco
AU - Forloni, Gianluigi
AU - Herrero Ezquerro, Maria Trinidad
AU - Noè, Francesco Mattia
AU - Pifferi, Fabien
AU - Ros-Bernal, Francisco
AU - Christensen, Ditte Zerlang
AU - Dix, Sophie
AU - Richardson, Jill C.
AU - Lamberty, Yves
AU - Drinkenburg, Wilhelmus
AU - Rossini, Paolo Maria
PY - 2013
Y1 - 2013
N2 - Different kinds of challenge can alter spontaneous ongoing electroencephalographic (EEG) rhythms in animal models, thus providing paradigms to evaluate treatment effects in drug discovery. The effects of challenges represented by pharmacological agents, hypoxia, sleep deprivation and transcranial magnetic stimulation (TMS) on EEG rhythms are here reviewed to build a knowledge platform for innovative translational models for drug discovery in Alzheimer's disease (AD). It has been reported that antagonists of cholinergic neurotransmission cause synchronisation of spontaneous ongoing EEG rhythms in terms of enhanced power of EEG low frequencies and decreased power of EEG high frequencies. Acetylcholinesterase inhibitors and serotonergic drugs may restore a normal pattern of EEG desynchronisation. Sleep deprivation and hypoxia challenges have also been reported to elicit abnormal synchronisation of spontaneous ongoing EEG rhythms in rodents. The feasibility and reproducibility of TMS have been demonstrated in rodents but information on a consistent modulation of EEG after TMS manipulation is very limited. Transgenic mice over-expressing human amyloid precursor protein complementary DNAs (cDNAs) harbouring the 'Swedish' mutation and PS-1 cDNAs harbouring the A264E mutation, which recapitulate some of the pathological features of AD, exhibit alterations of spontaneous ongoing EEG rhythms at several low and high frequencies. This does not appear, however, to be a consequence of beta-amyloid deposition in the brain. The present review provides a critical evaluation of changes of spontaneous ongoing EEG rhythms due to the experimental manipulations described above, in order to stimulate the promote more adherent models fitting dynamics in humans.
AB - Different kinds of challenge can alter spontaneous ongoing electroencephalographic (EEG) rhythms in animal models, thus providing paradigms to evaluate treatment effects in drug discovery. The effects of challenges represented by pharmacological agents, hypoxia, sleep deprivation and transcranial magnetic stimulation (TMS) on EEG rhythms are here reviewed to build a knowledge platform for innovative translational models for drug discovery in Alzheimer's disease (AD). It has been reported that antagonists of cholinergic neurotransmission cause synchronisation of spontaneous ongoing EEG rhythms in terms of enhanced power of EEG low frequencies and decreased power of EEG high frequencies. Acetylcholinesterase inhibitors and serotonergic drugs may restore a normal pattern of EEG desynchronisation. Sleep deprivation and hypoxia challenges have also been reported to elicit abnormal synchronisation of spontaneous ongoing EEG rhythms in rodents. The feasibility and reproducibility of TMS have been demonstrated in rodents but information on a consistent modulation of EEG after TMS manipulation is very limited. Transgenic mice over-expressing human amyloid precursor protein complementary DNAs (cDNAs) harbouring the 'Swedish' mutation and PS-1 cDNAs harbouring the A264E mutation, which recapitulate some of the pathological features of AD, exhibit alterations of spontaneous ongoing EEG rhythms at several low and high frequencies. This does not appear, however, to be a consequence of beta-amyloid deposition in the brain. The present review provides a critical evaluation of changes of spontaneous ongoing EEG rhythms due to the experimental manipulations described above, in order to stimulate the promote more adherent models fitting dynamics in humans.
KW - Alzheimer Disease
KW - Animals
KW - Anoxia
KW - Brain
KW - Disease Models, Animal
KW - Electroencephalography
KW - Mice
KW - Rats
KW - Sleep Deprivation
KW - Transcranial Magnetic Stimulation
KW - Translational Medical Research
KW - Alzheimer Disease
KW - Animals
KW - Anoxia
KW - Brain
KW - Disease Models, Animal
KW - Electroencephalography
KW - Mice
KW - Rats
KW - Sleep Deprivation
KW - Transcranial Magnetic Stimulation
KW - Translational Medical Research
UR - http://hdl.handle.net/10807/54062
U2 - 10.1016/j.clinph.2012.07.023
DO - 10.1016/j.clinph.2012.07.023
M3 - Article
SN - 1872-8952
VL - 124
SP - 437
EP - 451
JO - Clinical Neurophysiology
JF - Clinical Neurophysiology
ER -