DR. FYMAT was educated at University of Paris-Sorbonne and University of California at Los Angeles. He is President/CEO/Professor at International Institute of Medicine & Science with a previous appointment as EVP/COO/Professor at Weil Institute of Critical Care Medicine. Formerly, Professor of Radiology, Radiological Sciences, Radiation Oncology, Critical Care Medicine, and Physics at several U.S. and European Universities. He has published ~ 435 scholarly publications. As scientific organizing committee member and keynote speaker, he has lectured extensively in the USA, Canada, Europe, Africa, and Asia. He is Editor-in-Chief, Honorable Editor or Editor of 62 medical- scientific Journals to which he contributes regularly.

While researching Parkinson's disease (PD), Lewey discovered abnormal alpha-synuclein protein deposits in the brainstem where they disrupt brain's normal functioning by depleting dopamine, causing Parkinsonian symptoms. PD is a risk factor that speeds up decline in cognition leading to PD dementia (PDD). PDD and dementia with Lewy bodies (DLB) are but two forms of Lewy body dementias (LBD). In LBD, these abnormal proteins diffuse throughout other brain areas. Te brain chemical

acetylcholine depletes, causing disruption of perception, thinking and behavior. LBD exists either in pure form, or in conjunction with other brain changes, including Alzheimer's disease and PD. The diffuse form of the disease was only discovered in 1967 by Kenji Kosaka. Together with PD, multiple system atrophy, and other rarer conditions, LBD is classified as atypical parkinsonian syndrome. It is one of the synucleinopathies. I propose to review the mechanisms of action of LBD even though the exact cause of the disease - indeed the cause of all synucleinopathies - remains unknown. I will also analyze the signs/symptoms of the disease, its probable or possible diagnosis, supportive tests including

I-123 MBIG myocardial scintigraphy, and differential testing with regard to such nucleinopathies as PDD, PD, vascular dementia, multiple system atrophy, progressive supranuclear palsy, corticobasal palsy degeneration, and corticobasal syndrome. I will also review current disease management principles (pharmacological and otherwise). Lastly, I will outline current research programs and future strategies to modify the course of the disease using nimmunotherapy, gene therapy, stem cell therapy, and reducing amyloid-beta accumulations.