Emerging Concepts in Basic Science
After great success in 2016, this series highlighting basic dementia science will be a can't-miss aspect of AAIC 2017.
The Scientific Program Committee introduced the Emerging Concepts series, an innovative aspect of the AAIC program designed specifically for basic dementia science.
One Emerging Concepts session will be held each day from Sunday to Tuesday of the conference, concluding with a panel discussion on Wednesday that includes the three session leads.
The Emerging Concepts series will focus on three areas:
Sunday, July 16 | 2 – 3:30 p.m.
Lead: Roxana Carare
The failure of elimination of amyloid-beta (A) from the brain is key to the pathogenesis of Alzheimer’s disease (AD), resulting in the accumulation of A in the walls of arteries, as cerebral amyloid angiopathy. There are several mechanisms for the breakdown and clearance of A from the brain parenchyma and ageing as well as possession of Apolipoprotein E4 genotype appear to interfere with these mechanisms. Measuring the concentration of different cerebral proteins in the cerebrospinal fluid forms the basis of the CSF biomarker field and the exact routes of communication between the CSF and the brain parenchyma have received renewed attention in recent years. The failure of clearance of cerebral proteins is associated with inflammation. This symposium will address the vascular pathways for the clearance of proteins from the brain parenchyma and how they could be manipulated therapeutically. The inflammatory processes and the interaction between the cerebrospinal fluid and interstitial fluid compartments will be discussed within the context of vascular pathways of clearance of proteins and new experimental models and therapeutic strategies for AD
Monday, July 17 | 2 – 3:30 p.m.
Lead: Clive Holmes
Recent studies highlight the role of peripheral innate and adaptive immunity in the pathophysiology of Alzheimer’s disease (AD). Changes in peripheral innate and adaptive immunity occurring in response to peripheral inflammatory events have a direct influence on the brain’s immune response and other aspects of brain pathology in AD.
This series of lectures will examine aspects of both peripheral innate and adaptive immunity in AD, with a focus on the effects of systemic infections on brain pathology in both human studies and murine models of AD at different stages of the disease. We show evidence that changes in peripheral immunity modulate various aspects of disease pathology in AD including amyloid-β deposition, T-cell infiltration, the CNS innate immune response and alterations in the clinical course of the disease. The evidence suggests that in AD the central response to these peripheral challenges involves aspects of both innate and adaptive immunity and is likely to change over the time course of the disease. Possible immunotherapeutic strategies will be discussed.
Tuesday, July 18 | 2 – 3:30 p.m.
Lead: Michel Goedert
Frontotemporal lobar degeneration (FTLD) is clinically, pathologically and genetically heterogeneous, but affects predominantly the frontal and temporal lobes of the cerebral cortex. There are three main clinical syndromes (behavioural-variant frontotemporal dementia, semantic dementia and progressive non-fluent aphasia), three predominant histologies (involving Tau, TDP-43 and FUS) and three major genetic causes (mutations in MAPT, GRN AND C9orf72). In recent years, much progress has been made, resulting in a better understanding of the biology underlying the clinical syndromes of FTLD. This Symposium aims to reflect major recent developments. Bernardino Ghetti will give an overview of FTLD, linking the clinical syndromes with histology and genetics. Sjors Scheres will present the atomic structures of Tau filaments obtained by cryo-electron microscopy. They are the first such structures of an amyloid fibril and indicate paths towards novel diagnostics and therapeutics for Tauopathies.Masato Hasegawa will talk about the RNA-binding proteins TDP-43 and FUS and their roles in FTLD. TDP-43 inclusions are the most common pathological characteristic of FTLD. Chris Shaw will talk about frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) and the hexanucleotide expansions in C9orf72, the most recently identified and most common genetic cause of FTLD.
Wednesday, July 19 | 2 – 3:30 p.m.
Moderator: David Morgan, University of South Florida, United States
Roxana Carare, Michel Goedert and Clive Holmes will each summarize the Emerging Concepts in Basic Science sessions offered on Sunday through Tuesday. Karl Herrup will also provide his perspective, which will be followed by audience questions and panelist discussion in response to these questions. Virginia Man-Yee Lee and Julie Williams, as plenary speakers, will participate as panelists to provide additional insights and perspective.