In a tauopathy mouse model, overexpressing the receptor lowered ApoE, prevented microglial activation, and lessened neurodegeneration. LDLR—a drug target for neuroprotection?
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.
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.
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.
By interfering with Aβ fibril growth, prion and two other cell-surface proteins may drive production of smaller, more toxic, oligomers and protofibrils.
Though the first two trial arms were negative on cognition, gantenerumab’s strong effect on biomarkers led to an open-label extension.
Even without entering the brain, SARS-CoV-2 jolts the choroid plexus into signaling danger via inflammatory signals. Microglia, astrocytes, and neurons mount a response resembling that in neurodegenerative and chronic brain disorders.
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, ...
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 disease progression—but even they are aghast at the price and hope the drug 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.