Scientific Program

Conference Series LLC Ltd invites all the participants across the globe to attend 18th International Conference on Dementia & Alzheimer disease Rome, Italy.

Day 1 :

Keynote Forum

Gianna C. Riccitelli

Neuropsychology and Behavioral Neurology Research Unit, Lugano, Switzerland.


Time : 10:00-10:20

Dementia & Alzheimer disease International Conference Keynote Speaker Gianna C. Riccitelli photo

Gianna C Riccitelli is Private Docent from Faculty of Biomedical Sciences, University of Italian Switzerland, Lugan, Switzerland. She has completed her PhD and postdoctoral studies from San Raffaele Vita-Salute University, Milan, Italy. She is the scientific leader of Neuropsychology and Behavioral Neurology Research Unit of Neurocenter of Southern Switzerland, Lugano Civic Hospital. She has published more than 55 papers in reputed journals.


Today cognitive neurodegenerative diseases are a serious critical problem, with a prevalence that doubles every five years. Meanwhile, pharmacological therapies appear have no significant effect on disease course and cognitive training/rehabilitation interventions have generated temporary hope and mild proof of efficacy.Transcranial Magnetic Stimulation (TMS), one of the most popular non-invasive brain stimulation technologies, uses electrical fields generated in the brain to enhance the activity of key brain regions contributing to relevant cognitive processes.
Nevertheless, the therapeutic benefit and clinical significance of TMS remain inconclusive, due to lack of a sufficient number of double-blind, placebo-controlled, randomized clinical trials demonstrating enduring effects and positive impact on prognosis.
The field remains promising but, to make further progress, research efforts need to take into account the latest evidence of the anatomical and neurophysiological features underlying cognitive deficits in these patient populations.Moreover, as the development of in vivo biomarkers is ongoing, allowing for an early diagnosis of these neurocognitive conditions, one should consider a scenario in which TMS treatment will be personalized and made part of a cognitive rehabilitation program or used as a potential adjunct to drug therapies from the earliest stages of such diseases. Research should also integrate novel knowledge on the mechanisms and constraints promoting the impact of electrical and magnetic fields on cerebral tissues, and brain activity, and incorporate the principles of information-based neurostimulation.

Keynote Forum

Dr.Frédéric Checler

University of Nice-Sophia-Antipolis, France

Keynote: Aminopeptidase A and Dipeptidyl aminopeptidase 4 as putative targets in Alzheimer’s disease

Time : 10:20-11:20

Dementia & Alzheimer disease International Conference Keynote Speaker Dr.Frédéric Checler photo

F. Checler received his PhD in Cellular and Molecular Pharmacology from University of Nice-Sophia-Antipolis (1983). Since 1994, he works on neurodegenerative diseases where he was mainly interested in proteolytic dysfunction and cell death mechanisms involved in Alzheimer’s disease then on dysfunctions taking place in Parkinson’s and prion diseases.Nowadays, he is developing an additional project aimed at identifying common molecular pathways either exacerbated or disrupted in neurodegenerative diseases and cerebral cancer. F. Checler belongs to the laboratory of Excellence DistALZ(Development of Innovative STrategies for translational Approach in ALZheimer Disease). He was the first president of the “Ligue Européenne Contre la Maladie d’Alzheimer”.


Several studies indicated that pGlu3-Ab is toxic, prone to aggregation and serves as a seed of Ab that aggregates and accumulates in Alzheimer’s disease-affected brain. The cyclisation of the glutamate in position 3 requires prior removal of the Ab N-terminal aspartyl residue to allow subsequent biotransformation. We have identified aminopeptidase A (APA) and dipeptidyl peptidase 4 (DDD4) as the main exopeptidases involved in an additional manner in cells. This data derives from mass-spectrometry analysis as well as genetic depletion (shRNA) and pharmacological blockade by selective inhibitors). We will describe data en obtained by in vitro biochemical approach (mass-spectroscopy analysis), measurements of synaptic density (organotypic slices), Ab load (Elisa) and Ab positive lesions (immunohistochemistry) and behavioral studies (memory defects in transgenic mice). Importantly, we demonstrate that, concomitantly to the occurrence of pGlu3-42- Ab positive plaques, APA and DPP4 activity are augmented at early Braak stages in sporadic AD brains. We will discuss the potential benefit of targeting these proteolytic activities to fight Alzheimer’s disease.