First results from the Genetic FTD Initiative, and the advance of an HDAC inhibitor drug into Phase 2, made big splashes at the ICFTD conference held last month in Vancouver. Five hundred and ninety scientists from 30 countries met to exchange the latest clinical and scientific news on the diseases that make up FTLD. Multi-center cohort studies in Europe and North America reinforced the sense that there is a community spirit that may allow a common approach to how to develop therapies. Frontotemporal lobar degeneration can start in myriad ways—with social disinhibition, overeating, halting speech, or even odd misperceptions of pain or cold—but it always ends in dementia. Attendees said that the FTD field is poised for rapid progress.
As the first five of the nation’s 27 Alzheimer’s Disease Research Centers system marked their 30th birthday, one of them celebrated with a scientific conference at Massachusetts General Hospital. Blending the past, present, and future, scientists told stories of how the discovery of the first presenilin mutation today lives on in structural work to find better γ-secretase drugs, or how an overlooked gel band visible since the 1990s now hints at an unappreciated APP cleavage and adds a new twist to explore in BACE1 inhibitor drugs. Others summarized the latest on characterizing the Alzheimer’s prodrome and sharpening tools to target it in secondary prevention trials. Along the way, conference attendees learned that, laid out flat, the cortical mantle of the human brain is the size of a large pizza, a factoid that matters to understanding Alzheimer’s.
Clinical trials, brain imaging, biomarkers, and intervention studies drew more than 4,000 researchers to the Alzheimer’s Association International Conference 2014 at the Copenhagen Congress Center in Demark. Data from Phase 2 clinical trials of crenezumab, an anti-Aβ antibody, disappointed, but positive results from a large Finish intervention study raised hope that lifestyle changes can pay dividends toward preventing dementia. The Alzheimer's Prevention Initiative announced a new partnership with Novartis to test if an active Aβ vaccine or a BACE inhibitor can slow or prevent sporadic Alzheimer's in people who are genetically predisposed to the disease.
So you think Alzheimer’s is a neuronal disease? Well, yes, but you might as well think again. Even as the amyloid hypothesis is growing stronger with human genetics and longitudinal biomarker studies, decades of neurocentric research have given way to a broader appreciation that Aβ and tau intersect with the glial and vascular system and are subject to new forms of genetic regulation in the aging brain. What’s more, parabiosis shows that the blood itself carries signals into the brain that can powerfully influence its aging and degeneration. These topics dominated the first Zilkha Symposium on Alzheimer’s Disease and Related Disorders, hosted on April 4 by the University of Southern California.
More than 200 researchers braved dizzying altitude, howling coyotes, and a fairly brooding mood in light of elusive trial success, to exchange the latest on Alzheimer's and Parkinson’s diseases in joint symposia held March 2-7 in Keystone, Colorado. Between plenary and parallel talks, bustling poster sessions, and the odd foray to the slopes, scientists discussed trial design, genetics, pathology, biomarkers, and cell and protein biology. Check back in the coming week as Alzforum posts highlights.