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Background It is well-known that compared to normal elderly (Nold) subjects, patients with dementia due to Alzheimer’s disease (ADD) manifest ten times convulsive seizures. The present study tested the different features of the resting state eyes-closed electroencephalographic (rsEEG) rhythms in a group of patients with mild cognitive impairment due to AD and interictal epileptiform discharge (ADMCI IED+), compared to groups of ADMCI patients without interictal epileptiform discharge (ADMCI IED−), ADD patients, and Nold subjects. Methods Clinical, neuropsychological, and rsEEG data, in 30 Nold, 31 ADMCI IED−, 11 ADMCI IED+, and 30 ADD subjects were available in an international archive. Individual alpha frequency peak was used to determine the delta, theta, alpha1, alpha2, and alpha3 frequency band ranges. Fixed beta1, beta2, and gamma bands were considered. eLORETA estimated the rsEEG cortical sources in EEG segments free from artifacts and IED. The analysis of the area under the receiver operating characteristic (AUROC) curve computed the classification rate. Results Compared to the Nold group, the ADMCI IED−, ADMCI IED+ and ADD groups presented higher widespread delta source activities and lower posterior alpha source activities. As novel EEG results, compared to the ADMCI IED- group, the ADMCI IED+ unveiled higher frontal and temporal delta source activities. Furthermore, temporal delta source activity allowed a good classification (AUROC > 0.85) between the ADMCI IED− and ADMCI IED+ individuals. Conclusions In quiet wakefulness, the abnormalities in cortical neural synchronization underpinning brain arousal at delta frequencies are higher in the ADMCI IED+ than the ADMCI IED− subjects.

The pathological process of Alzheimer's disease (AD) starts years before the appearance of clinical symptoms. The understanding of those mechanisms at the basis of such long phase will permit the development of new drugs to counter neurodegeneration before irreversible neuronal losses occur. Ideally, the development of such drugs should be based on the markers of disease progression homologous in humans and animals. The perfect experimental model recapitulating the main pathological characteristics of AD has yet to be engineered, but available models address a number of pathological AD features allowing to translate human markers to mice. The present paper is an overview of the neuroimaging markers used to map AD-like pathology and its progression in vivo in mice models of amyloidosis. Mice models are widely used to test AD candidate drugs and to predict their effects in human. Therefore, the crucial key is the identification of AD progression imaging markers homologous to those validated in early AD patients.

Novel proapoptotic Smac mimics/IAPs inhibitors have been designed, synthesized and characterized. Computational models and structural studies (crystallography, NMR) have elucidated the SAR of this class of inhibitors, and have permitted further optimization of their properties. In vitro characterization (XIAP BIR3 and linker-BIR2-BIR3 binding, cytotox assays, early ADMET profiling) of the compounds has been performed, identifying one lead for further in vitro and in vivo evaluation.