NTX XIX: NINETEETH INTERNATIONAL NEUROTOXICOLOGY CONFERENCE

II.   PERSPECTIVE AND KEYNOTES.

III.    PARKINSONISM TUTORIALS. The objective of the tutorial session is to provide a scientific background for the more detailed sessions to follow. Tutorials will include a Historical Overview, Dopaminergic Systems and a Gene Primer. This session is expected to provide a unifying framework and rationale for the entire conference.

IV.    CLINICAL AND NEURO-PATHOLOGICAL FEATURES. This section will not only provide a general introduction to clinical and pathological features of Parkinson’s disease; perhaps more importantly, it will address timely and controversial issues that include (I) the definition of idiopathic Parkinson’s disease vs. parkinsonian syndromes, (II) similarities and differences between genetic and sporadic idiopathic parkinsonism, (III) early- vs. late-onset parkinsonism, and (IV) role and importance of Lewy bodies.

V.    EPIDEMIOLOGICAL STUDIES: RISK FACTORS.

This section will discuss clues from epidemiological studies that may help to identify risk factors involved in the pathogenesis of human parkinsonism. This includes (I) results of large population-based investigations, (II) data from twin’s studies, (III) the potential roles of pesticides and metals, and (III) cigarette smoking and caffeine intake as inversely associated with the incidence of parkinsonism.

VI.    ENVIRONMENTAL RISK FACTORS. In this session, specific agents will be discussed as potential neurotoxicants targeting the nigrostriatal system. Examples include thio-carbamate, organochlorine and rotenoid derivatives. Correlation of basic research evidence with epidemiological data will be emphasized together with potential mechanisms of action.

VII.    GENERAL NEUROTOXICOLOGY POSTER SESSION. Presentation of papers from poster and informal discussion are a highlight of this meeting. Free communications from poster on any topic of neuroscience and toxicology are welcome. All papers in competition for the Student Awards will be presented form poster.

VIII.    DISCUSSION GROUP: CLINICAL DIAGNOSIS ISSUES. Important themes which emerged from the day’s sessions will be further elaborated with the intent of providing diagnostic guidelines for the correct dentification and classification of the parkinsonian phenotype by clinicians and researchers.

IX.   GENETIC RISK FACTORS. Data pointing to a genetic predisposition underlying the etiology of human parkinsonism will be reviewed in this section. Clues from familial cases of parkinsonism will be discussed. Emphasis will also be given to new genetic methodologies for the identification of specific risk factors and the use of transgenic animal models.

X.   DEVELOPMENTAL EXPOSURE AND PARKINSONISM. In this session, we will discuss early exposure to environmental toxicants and implications for delayed and long-term effects. We will focus discussion on the possibility that environmental risk factors as a fetus or child could trigger vulnerability to Parkinson’s disease later in life.

XI.    DISCUSSION GROUP: GENES VS. ENVIRONMENT. In this session, new theories on the role of genetic and environmental risk factors in human parkinsonism will be discussed on the basis of emerging evidence from epidemiological, clinical and basic research.

XII.    MECHANISMS OF PARKINSONISM. Mechanisms by which environmental and genetic risk factors may ultimately play a role in the pathogenesis of nigrostriatal degeneration will be discussed. Common toxic pathways that may be triggered by both environmental insults and genetic abnormalities will be identified. Because of its relevance for both familial and sporadic parkinsonism, mechanisms of a-synuclein-induced pathology will be reviewed and updated.

XIII.    BIOMARKERS AND MODELS OF PARKINSONISM. Better biomarkers, that is, reliable indicators of risk, disease state, and disease severity, would accelerate research on the causes and progression of Parkinson’s disease and the development and testing of therapies. Non-human models of Parkinson’s disease are essential for understanding the causes and progression of nerve cell death and for efficiently developing new therapies.

XIV.    THERAPEUTIC APPROACHES. Based on our current knowledge of neurodegenerative mechanisms and pathways that underlie the parkinsonian phenotype, novel strategies for the treatment of the disease will be evaluated in this final section. Both medical and surgical approaches will be considered including (I) antioxidants, (II) neurotrophic factors, (II) deep brain stimulation, and (IV) the use of stem cells.

XV.   FINAL PANEL DISCUSSION AND RECOMMENDATIONS. The objective of this final session is not only to summarize important outcomes of the conference, but also to identify critical gaps in our knowledge of Parkinson’s disease and exciting new research avenues. The importance of an interdisciplinary approach bridging experimental and clinical efforts will be emphasized.