Trial data for aducanumab did not answer key questions, such as how long patients should stay on drug, leaving clinicians around the world to struggle with practical and ethical issues.
Physicians have a new Alzheimer’s treatment option, but most clinics are not ready to administer it. Questions remain about eligibility and insurance, to say nothing of clinician and infusion capacity.
Many Alzheimer’s researchers believe the aducanumab approval heralds the beginning of treatments that slow underlying disease progression—but even they are aghast at the price and hope it will not sideline other trials.
Industry analysts and watchdogs have heaped criticism on the FDA, while Alzheimer’s researchers remain divided over whether the decision helps or harms the field.
In mice, disease-associated microglia proliferate so much that they become senescent. Plaques then run amok and synapses are lost.
The anti-tau immunotherapy did not slow cognitive decline among people in the earliest stages of AD, nor did it evoke changes on tau-PET scans.
In the face of aging or amyloidosis, microglia lacking C9ORF72 ramped up interferon genes, accumulated lysosomes, and ate synapses.
The tau vaccine evoked a robust anti-tau antibody response, which curbed the rise in plasma NfL and CSF p-tau over two years. Cognitive decline continued.
Virtual Exhibit Hall
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome F. Hoffmann-La Roche, joining our other exhibitors — Biogen, BioLegend, Abcam, BrainXell, and the Jackson Laboratory.
Fallout Continues After Aducanumab Approval
Two weeks after the FDA gave the nod to aducanumab, the aftershocks continue to reverberate. Critics are lambasting the agency, three members of its advisory committee resigned, and the drug’s cost has ignited calls for pricing reform. Meanwhile, Alzheimerologists are split, with some applauding the first disease-modifying therapy and others worrying it could dampen research into other drugs. All bemoan the broad label and agree that the drug’s clinical rollout will be challenging. Take in a 360-degree view of this sea change in the Alzheimer’s field in Madolyn Rogers’ four-part series.
In C9ORF72 knockout mice, microglia transform from helping neurons to hindering synapses, according to a new study. C9-less microglia ramped up interferon response genes with age, and in a mouse model of amyloidosis, loss of C9 stoked microglial clean-up of plaques. Alas, the glia devoured synapses, too, and the mice became forgetful.
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