AAIC Roundup—All the News From Toronto

Alzforum has concluded coverage of the Alzheimer’s Association International Conference with a story on the sensitive issue of disclosing biomarker and genetic risk data to thousands of cognitively healthy people who enroll in secondary prevention trials. The story rounds out 18 stories on the major themes that emerged at the meeting, held July 22-28 in Toronto. You can browse the series, or print a pdf to peruse at your leisure.  

Few clinical trials reported data. The failure of the first anti-tau therapy that made it to Phase 3 attracted heat for the way the data was presented (see Jul 2016 conference news). The PreDiva multi-domain intervention trial fell short, but gave subtle hints that targeting hypertension might stem cognitive decline (see Aug 2016 conference news). Researchers seemed encouraged by Phase 1 data of new BACE inhibitors, and voiced mixed feelings about LY3002813, the first therapeutic antibody that specifically targets pyroglutamylated Aβ (see Aug 2016 conference news). 

In contrast, scientists were enthusiastic about new initiatives around the globe that are targeting asymptomatic people for secondary prevention trials. Three AAIC stories summarize how the Global Alzheimer’s Platform and the European Prevention of Alzheimer’s Disease work as public-private partnerships to tap into patient registries, health plans, and other large cohorts of aging people to identify those most at risk and likely to benefit from early intervention (see Aug 2016 conference news). 

GAP and EPAD are starting up following DIAN and API, which have been studying autosomal-dominant and ApoE4-homozygous cohorts for many years and are churning out data. A five-part AAIC report narrates how far these more mature initiatives have come. Topics include DIAN’s increasingly connected participant community, the network’s worldwide expansion, new data quantifying subtle cognitive decline earlier than previously known, and the start of tau imaging. Importantly, a new project is comparing DIAN and LOAD data to establish how ADAD and LOAD may differ—or not. As data roll in, ethical and privacy issues about how best to publish and share this data set are coming to the fore (see Aug 2016 conference news). 

Researchers praised a new staging scheme for dementia. Called ATN—short for amyloid, tau, and neurodegeneration—it separates tau pathology from other markers of neuronal decline, such as hippocampal atrophy (see Aug 2016 conference news). The ATN scheme may help researchers define SNAP, aka suspected non-Alzheimer’s pathology, which manifests hints of neurodegeneration without Aβ pathology and, surprisingly to some, also largely without tau pathology. Advances in tau imaging will help in this regard. In Toronto, researchers presented new tau tracers that may be more specific for neurofibrillary tangles. Multimodal imaging data correlating tau and Aβ accumulation supported the idea that aggregates of tau begin to spread through the cortex only after amyloid plaques have accumulated, and that atrophy follows tau (see two-part conference news). 

Researchers have begun using longitudinal amyloid PET data to estimate how fast Aβ accumulates over decades and to identify areas of the brain, such as the striatum, where the Aβ load may be valuable for prognosis (see Aug 2016 conference news). Other imaging modalities emerged as potential diagnostic tools. Scientists study how fading connectivity patterns among neurons may portend amyloid and tau pathology, suggesting that network disruptions fuel protein aggregation (see Aug 2016 conference news). Last but not least, geneticists are linking genetic variation with disease endophenotypes, such as amyloid plaques, neurofibrillary tangles, and brain atrophy. Several presentations coalesced around the idea that there are distinct genetic variants that link to specific pathologies (see Sep 2016 conference news).—Tom Fagan, Madolyn Rogers, and Gabrielle Strobel

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References

Conference Coverage Series Citations

  1. Alzheimer's Association International Conference 2016

News Citations

  1. In First Phase 3 Trial, the Tau Drug LMTM Did Not Work. Period.
  2. New Ways to Target Aβ and BACE Show Promising Phase 1 Data
  3. Coming to a Center Near You: GAP and EPAD to Revamp Alzheimer’s Trials
  4. At Age 8, DIAN Is Churning Out Data and Growing into a Movement
  5. Staging of Alzheimer’s, the Second: Neurodegeneration Does Not Equal Tauopathy
  6. Tau PET Studies Agree—Tangles Follow Amyloid, Precede Atrophy
  7. Refining Models of Amyloid Accumulation in Alzheimer’s Disease
  8. Homing in on Early Alzheimer’s Biomarkers: Does Connectivity Hold the Key?
  9. Amyloid and Neurodegeneration Have Different Underlying Genetics

Other Citations

  1. pdf

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