Scientific Program

Conference Series LLC Ltd invites all the participants across the globe to attend 12th World Congress on Dementia and Alzheimer Rehabilitation Stockholm, Sweden.

Day 1 :

Keynote Forum

Robert Hedaya

Georgetown University, USA

Keynote: Reversing SCI, MCI and early dementia using functional medicine

Time : 10:00 AM-10:40 AM

Euro Dementia 2019 International Conference Keynote Speaker Robert Hedaya photo

Robert J. Hedaya, MD, ABPN, CFM, DLFAPA  is board certified in psychiatry and psychopharmacology, and pioneered functional medicine in the neuro-psychiatric field. as clinical professor of psychiatry at Georgetown University medical center, he teaches courses including psycho-neuro-immuno-endocrinolgy. He is a faculty member at the institute for functional medicine, author of three books, and the founder of the national center for whole psychiatry. Dr. Hedaya is an editorial volunteer for advances in mind-body medicine and alternative therapies in health and medicine, has been featured in national media, and is a nationally and internationally recognized speaker.


It is widely recognized that the current treatment approach to subjective and mild cognitive impairment (SCI, MCI) and early dementia offers little in the way of efficacious treatment. Decades of research based on various linear models (e.g.,amyloid,acetylcholine) with targeted pharmaceutical treatments have failed to produce clinically meaningful results. On the other hand, basic science and systems biology have identified and elucidated multiple modifiable (and mutually interacting) pathophysiological systems which increase vulnerability to neurodegenerative disorders such as SCI, MCI and various dementias. The majority of cases of dementia are not unitary in etiology, but rather involve disturbances of multiple systems and are thus pathophysiologically impure. Even such APOE4 homozygotes generally have multiple contributing pathophysiologies. The etiological imprecision of our diagnostic terminology and continued use of a linear medical paradigm results in dismissal of relevant and modifiable pathophysiological contributors to dementia. Hence, diagnostic imprecision must be replaced with etiological precision.  Underlying pathophysiological processes which are involved in cognitive decline include: central insulin resistance, mitochondrial and oxidative dysfunction, loss of trophic (nutrient, hormonal, immune, enrichment) support, immune dysfunction and infection, toxicity, cardio-vascular dysfunction, trauma, structure and lifestyle. The clear association between these pathophysiologies, their clinically measurable biometric parameters, and cognitive decline provides a clear treatment map which is being used to reverse SCI, MCI and early to mid-stage dementia. A large trial of the Functional Medicine method is currently funded. This presentation will review the evidence and a series of cases demonstrating stabilization and recovery of cognitive function in these disorders.

Keynote Forum

Romeo Vitelli

The Canadian and American Psychological Associations, Canada

Keynote: When is a head injury more than a head injury? TBI and dementia in seniors

Time : 11:00 AM-11:40 AM

Euro Dementia 2019 International Conference Keynote Speaker Romeo Vitelli photo

Romeo Vitelli, C. Psych., is a registered psychologist in the Province of Ontario with areas of competence in clinical neuropsychology and forensic psychology. He received his doctorate from York University in 1987 and has been a registered psychologist since 1988. Along with being an active blogger with the Huffington Post and Psychology Today, he is also the author of three books and is a member in good standing of the International Neuropsychological Society and clinical neuropsychology divisions of "The Canadian and American Psychological Associations".


Though traumatic brain injury (TBI) has been widely recognized as a leading cause of death and disability around the world, there is still considerable controversy about the potential role it plays in the development of later cognitive, including Alzheimer's disease (AD). Despite this controversy, research has shown that even a single moderate to severe head injury can lead to increased amyloid-beta (A) plaques and neurofibrillary tangles, two of the hallmark signs of AD. Also, a recent study looking at autopsy-confirmed dementia cases found that a substantial percentage of recorded cases have a prior history of head injury. In particular, older adults reporting a moderate to severe head injury involving loss of consciousness began showing symptoms of dementia three years earlier than participants with no history of TBI. Even when controlling for other factors such as lifetime history of depression, family history of dementia, level of education, and medical history, the link between dementia and TBI remains strong.  Though more research is needed to explore the TBI-dementia link, health care and legal professionals need to be aware of the increased risk faced by older adults recovering even from accidents that may not be considered serious by objective standards.This includes the often thorny problem of proving causality in dementia cases arising from injuries sustained in slip and fall cases, automobile accidents, elder abuse, and other instances involving mild to moderate concussion. A recent case study will be presented to help demonstrate the legal and medical ramifications of dementia symptoms in a head-injured older senior.

Keynote Forum

Panteleimon Giannakopoulos

University Hospitals of Geneva, Switzerland

Keynote: Amyloid deposition in brain aging: Causal agent or innocuous bystander?

Time : 11:55 AM- 12:35 PM

Euro Dementia 2019 International Conference Keynote Speaker Panteleimon Giannakopoulos photo

Professor P. Giannakopoulos completed his medical studies at the University of Athens where he graduated in 1988. His psychiatric training was performed clinically in London (Maudsley Hospital) Geneva and Paris. He is a professor and department head in department of the Geneva University Hospitals of psychiatry since 1998. Promoted to full professor in 2004, he is head of the department of psychiatry hospital and assistant dean in charge of postgraduate education in the faculty of medicine. Since 2006, he serves on the executive committee and the board of directors of the HUG (University Hospitals of Geneva). In 2008, he received the distinction of Commander of the Order of the Phoenix in his country of origin.


PET amyloid imaging has been initially considered as the main tool to investigate the beginning of the AD process in cognitively intact individuals. The percentage of PET-amyloid positive controls is of 6% at age 60 but reaches 50% at age 90 in community-based sample pointing to the fact that amyloid deposition (as amyloid plaque formation) is closely related to aging process. In fact, increased PiB binding has been reported in almost 20%-30% of cognitively preserved elders mainly in posterior cingulate cortex, precuneus and prefrontal cortex. Compared with amyloid-negative, amyloid-positive controls showed moderate decline in verbal and visual episodic memory over 36 months but no changes in non-memory functions. Most importantly, the absence of amyloid in MCI cases is associated with cognitive stability at 36 months. Increased PET-PiB binding is associated with brain atrophy, cortical thinning but also decreased cortical metabolism, aberrant functional connectivity at rest and decreased task-related deactivation of the default mode network. Altogether these data suggest that contrasting with CSF Aß and tau changes that sign a biological diathesis to neurodegeneration, amyloid positivity in the human brain is present as a part of the aging process representing a critical step preceding the installation of AD pathophysiology. However, not all cases with elevated PET-PiB bindings evolve to AD and several cases develop dementia not necessarily related to amyloid aggregation.Several recent contributions revealed that neurodegeneration takes place without a temporal link with fibrillar amyloid deposits. Alternative but less frequent pathways exist starting from tau deposition with modest Aß pathology.