BIOMEDICAL MEETINGChair: Teepu Siddique, Northwestern University Feinberg School of MedicineComing full circle in the era of molecular pathology:In the nineteenth century Charcot summarized the principal anatomic pathology of ALS as degeneration of upper and lower motor neurons. It is obvious from his description that neurons of the motor system bear the brunt of the pathology, but implicit in his description is that while motor system neurons degenerate, supporting cells proliferate, hence the sclerosis. In late 20thcentury we moved from this unity of pathology to diversity of etiology. This suggested that ALS was composed of a myriad of disease entities, each requiring its own treatment. The enormity and complexity of this task was daunting. Research in the early 21stcentury has provided some relief in this regard. It has begun to show that although ALS does not have a common etiology; downstream pathways of molecular pathology are shared. Even more interesting are the observations that these or similar molecular pathologies operate not just in ALS, but also in other neurodegenerative diseases. 2011 was the year of the gene. The discovery of the expanded hexanucleotide repeat in C9ORF72 explained the etiology of many cases of familial ALS and provided a unifying etiology to most cases of familial ALS/FTD. The discovery of ubiquilin2 and P62 provided unifying molecular pathologies of ALS, ALS/dementia and other manifestations of neurodegeneration. Implications of these observations are that we can have the same etiology give rise to different phenotypes and some pathological elements are common to different phenotypes. What then defines phenotype? Molecular pathology and topographical microscopic anatomy of the nervous system must then define the phenotype of neurodegenerative diseases such as ALS, FTD, Parkinson disease, and Alzheimer disease. The identification of common functional elements in the downstream molecular cascade provides new underpinnings of commonality. Thus, diverse etiologic streams, both genetic and acquired, appear to flow into the same great river to give rise to neurodegeneration. However, this great river may course through different landscapes, shaping the phenotype. So, recent advances in pathogenesis are moving ALS research from famine to feast, and we are now confronted with major imperatives that are the essence of ALS. The ALS/MND 2012 symposium in Chicago will be very interesting and exciting as we struggle to reconcile new data, necessitating adjustments in our understanding of ALS and other neurodegenerations. We will hear from our colleagues how these new findings help us understand the basic molecular pathology of ALS and dementias, and more importantly, how we can agree in order to move forward from understanding to application, from reduction to synthesis, and from accurate diagnosis to rational therapy.
Proposed platform session themes include:- Small Molecule Screening
- Epigenetics
- Proteasomes
- Cellular implications of RNA repeat expansions
- Astrocyte function
- Animal models: what do we want from these models, neurophysiology and biochemistry
- Protein Aggregation
- RNA processing session
- Stem cell biology
CLINICAL MEETINGChair: Robert Sufit, Northwestern University Feinberg School of MedicineThe enthusiasm of the ALS/MND community that gathered in Sydney was palpable. To quote from last year’s call for abstracts: ‘Recent years have witnessed a surge of interest across the ALS/MND landscape around the world. The discovery of causal genes linked to the development of familial ALS/MND and advances in our understanding of disease pathogenesis more generally, have re-ignited research interest. Problems related to clinical heteroge |