CONFERENCE COVERAGE SERIES
AAT-AD/PD™ 2020 Conference: Advances in Alzheimer's and Parkinson's Therapies
Virtual Meeting
02 – 05 April 2020
Caught amid COVID-19, the organizers of this meeting decided on March 10, 2020, to switch to a virtual format. It offered prerecorded lectures and e-posters, as well as livestreamed discussions, “Meet-the-Professor” audio chats, and a virtual exhibit hall. New data included widely anticipated results of the DIAN-TU clinical trial of solanezumab and gantenerumab, and of robust phospho-tau plasma tests. The online stream also brought new data on a range of trials against tau, α-synuclein, and other targets in age-related neurodegenerative disease, and on pathogenesis and other topics.
New Assay, New Cohorts—Plasma p-Tau181 Looks Even Better
At AAT-ADPD, researchers report how they built on prior reports that a person’s blood level of p-tau181 tells if they have Alzheimer’s.
217—The Best Phospho-Tau Marker for Alzheimer’s?
P-tau217 appears sooner than p-tau181 in the brain, and it distinguishes AD from controls and other dementias even more cleanly.
In DIAN-TU, Gantenerumab Brings Down Tau. By a Lot. Open Extension Planned
Data shown at AAT-AD/PD explain why the DIAN-TU trial missed its primary endpoint. But gantenerumab strongly reduced plaques, tau, phospho-tau, and slowed NfL. This result prompted an open-label extension, sustaining hope for efficacy.
Confused About the DIAN-TU Trial Data? Experts Discuss
The AAT-AD/PD conference hosted a virtual conversation about what the trial’s disappointing cognitive and tantalizing biomarker data might mean. Hidden between thank you’s and pledges to stay committed were substantive points of debate and context.
Active Tau Vaccine: Hints of Slowing Neurodegeneration
In a Phase 2 trial, the vaccine reportedly normalized the rise in plasma NfL, and appeared to lower CSF tau and retard brain atrophy.
Non-Aβ, Non-Tau Drugs Tweak Markers, Cognition in Alzheimer’s, Huntington’s
Researchers at the online AAT-AD/PD meeting touted therapies that target neuroinflammation, synapses, epigenetic regulation, or the cortisol stress response.
Does Alzheimer’s Start in the Heart of the Cholinergic System?
In people with Alzheimer’s biomarkers, the basal forebrain shrinks early, foreshadowing microglial neurotoxicity, atrophy in the medial temporal lobe, and cognitive decline.
‘Working from Home’: Do Gut Microbes Hold Sway Over Glia, Aβ?
Scientists report at AAT-AD/PD that they tightened a causal connection between gut microbes, microglial function, and protein deposits. In mice, that is.
Aβ in Lewy Body Disease: Two Diseases at Once, or Another Beast Entirely?
For people with Parkinson’s, carrying Alzheimer’s genetic risk variants upped their odds of harboring Aβ and tau pathology and getting dementia. In people with DLB, Aβ plaques worsened tau and Lewy pathology, and cognition.
With TREM2, Timing Is Everything
In a mouse model of amyloidosis, human wild-type TREM2 kept Aβ deposition at bay early on, but this defense became overwhelmed as plaques grew. The R47H AD risk variant never offered protection early on, and made things worse later.
Parkinson's Therapies Seek to Stem Progression
Trialists are shooting new arrows at the disease, including compounds that tweak autophagy, neuroinflammation, and glycolipid recycling.
α-Synuclein Antibody Misses Primary, May Have Signal on Secondaries
The first topline Phase 2 results from an antibody targeting Parkinson’s pathology, Roche’s prasinezumab, were a mixed bag. Next steps are unclear.