**3.1 EEG and EP**

Several quantitative electroencephalography (qEEG) studies have reported a progressive slowing of EEG and significant increased power in lower frequencies (delta and theta) in patients with AD [Prichep et al., 1994; van der Hiele et al., 2007]. In normal brain, correct performance in cognitive tasks implicate high levels of alertness and attention [Sala and Courtney, 2009], both dependent on the occurrence of fast EEG rhythms [Steriade, 2000, 2006].

EEG architecture shows great similarities across species. As above described, alertness is associated with fast frequencies in the EEG (e.g., beta activity), whereas non-REM sleep and drowsiness are characterized by slower waves (synchronized firing of cortical neurons).

Many experimental works have shown that drugs affect EEG characteristics in humans and rodents in a similar manner [Dimpfel et al., 1992; Jongsma et al., 1998a,b Coenen and Van Luijtelaar, 2003; Dimpfel, 2005]. In addition, a substantial body of studies suggest a relation between memory performance and EEG. For example, scopolamine decreases arousal level, which in turn increases EEG theta activity and impairs cognitive performance in object recognition in rodents. On the contrary, cholinergic agonists are able to decrease theta power and increase arousal.

6 Advances in Object Recognition Systems

In patients with AD, the profound cognitive deficits, following loss of basal cholinergic neurons, is likely due to disrupted cortex-hippocampus neuronal network [Whitehouse e al.,

Although in the last decades there has been considerable progress in understanding the molecular and cellular changes associated with Alzheimer's disease, to date, treatment of AD is merely palliative. In fact, medication with cholinergic drugs can only alleviate clinical symptoms, even if recent fMRI studies have shown the importance of cholinesterase

The recent understanding in AD pathogenesis has resulted in identification of a large number of new possible drug targets. These targets include therapies that aim to prevent production or remove the amyloid-β protein that accumulates in neuritic plaques, to prevent the hyperphosphorylation and aggregation into paired helical filaments of the microtubule-

Experimental approach to pathophysiological comprehension of human disease, as well as to new therapeutics, has ethical limitations in medicine. For this reason, design and development of acceptable *in vivo* experimental animal models is important in research.

However, many different experimental approaches and behavioral testing have been suggested to study learning and memory. In particular, neuropharmacological research, involved in discovery of new antidementia agents, needs good experimental models of disease as well as good behavioral tests, which are important to validate pharmacological

Several quantitative electroencephalography (qEEG) studies have reported a progressive slowing of EEG and significant increased power in lower frequencies (delta and theta) in patients with AD [Prichep et al., 1994; van der Hiele et al., 2007]. In normal brain, correct performance in cognitive tasks implicate high levels of alertness and attention [Sala and Courtney, 2009], both dependent on the occurrence of fast EEG rhythms [Steriade, 2000,

EEG architecture shows great similarities across species. As above described, alertness is associated with fast frequencies in the EEG (e.g., beta activity), whereas non-REM sleep and drowsiness are characterized by slower waves (synchronized firing of cortical

Many experimental works have shown that drugs affect EEG characteristics in humans and rodents in a similar manner [Dimpfel et al., 1992; Jongsma et al., 1998a,b Coenen and Van Luijtelaar, 2003; Dimpfel, 2005]. In addition, a substantial body of studies suggest a relation between memory performance and EEG. For example, scopolamine decreases arousal level, which in turn increases EEG theta activity and impairs cognitive performance in object recognition in rodents. On the contrary, cholinergic agonists are able to decrease theta

associated protein tau and, finally, to keep neurons alive and functioning normally.

On which basis can we build an experimental model of Alzheimer's disease?

1981; Coyle et al., 1983; Davies et al., 1987].

activity of drugs.

**3.1 EEG and EP** 

2006].

neurons).

power and increase arousal.

inhibitors (AChEIs) in treating AD [Miettinen et al., 2011].

Moreover, evoked potentials (EPs) show great correspondence between different species. In fact, auditory stimuli reveal a strong correspondence between rats and humans [Sambeth et al., 2003, 2004]. In both species, the short latency EP components are related to the processing of the physical properties of a stimulus, whereas the later components are associated with more endogenous processing (e.g., the psychological processes involved in the stimulus event) [Sambeth et al., 2003].

A particular aspect fascinate researchers: how does brain encode novel experiences, which are the intricate neural basis of learning and memory?
