Aducanumab Approval Sparks Backlash
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.
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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.
Many Alzheimer’s researchers believe the aducanumab approval heralds the beginning of treatments that slow disease progression—but even they are aghast at the price and hope the drug will not sideline other trials.
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.
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.
Though the first two trial arms were negative on cognition, gantenerumab’s strong effect on biomarkers led to an open-label extension.
By interfering with Aβ fibril growth, prion and two other cell-surface proteins may drive production of smaller, more toxic, oligomers and protofibrils.
Using isotope labeling and mass spectrometry imaging, researchers detail how plaques first assemble with an Aβ1-42 core, expand, then subsume Aβ1-38. Plaques start in cortex, then spread to hippocampus.
When you show a monkey an image of a familiar visage, a specialized cluster of face neurons in the monkey’s temporal pole fire rapidly. Their activity could explain the split-second speed of familiar face recognition.
Compared to amyloid PET and cortical thickness, tau PET better foretold waning cognition across the Alzheimer's disease spectrum, from cognitively normal to dementia. Age, but not sex or APOE status, hastened deterioration over two years.
In a tauopathy mouse model, overexpressing the receptor lowered ApoE, prevented microglial activation, and lessened neurodegeneration. LDLR—a drug target for neuroprotection?
In cultured neurons, these types of spines contain similar amounts and distributions of synaptic proteins, but mushroom spines boast more secretory and trafficking proteins, forging stronger synapses. And, holy moly, the videos!
Scientists linked genetic risk variants with protein changes in Alzheimer’s brain, cerebrospinal fluid, and plasma. They identified known drugs that target some of them.
Typically a sign of viral infection, double-stranded RNAs were spotted in C9ORF72 carriers, in whom they mingled with cytoplasmic TDP-43 inclusions. In mice, dsRNAs spread between connected neurons, provoking Type I interferon response and killing cells.
Interleukin-3, produced by astrocytes in the brain, helps microglia corral amyloid plaques in Alzheimer’s.
In carriers of the allele, cognition falters a bit earlier than in noncarriers. Brain amyloid, structure, and metabolism changed, as previously seen in sporadic and familial AD, but only some of the fluid markers did.