FDA Will Regulate Diagnostic Tests. Yes, Those for Alzheimer’s, Too.
Blood and other in vitro assays will need to meet the same standards as medical devices, including demonstrating diagnostic accuracy.
Blood and other in vitro assays will need to meet the same standards as medical devices, including demonstrating diagnostic accuracy.
By age 65, nearly all people who carry two copies of APOE4 harbor neuropathological or biomarker evidence of AD pathology.
In mice and cultured human neurons, PLCγ2 knockdown thinned out synapses and suppressed neuron firing. Rare loss-of-function PLCγ2 variants hike AD risk 10-fold.
People who had a damaged locus coeruleus accumulated tangles in their medial temporal lobes over the next three years, and their cognition declined.
Known for shuttling APP, the endosomal receptor latches on to tau. Knocking it down in glia reduced tau seeding. The N1358S risk variant ramped it up.
First papers from MoTrPAC initiative report myriad responses to endurance training in multiple organs in rats, including the brain and heart.
In the DIAN familial AD prevention trial, plaque-busting antibody gantenerumab, but not monomer-targeting solanezumab, nudged fluid markers toward normal.
Tauopathy cranks up lipid synthesis in neurons, which slip the fats to microglia. Blocking AMP kinase greases this process.
A new study argues that APOE4 homozygosity represents a genetically determinant form of AD, as opposed to a mere risk factor. By age 65, most people with two copies of the variant have amyloid plaques brewing in their brain. The authors believe APOE4 homozygotes should be considered similar to people with autosomal-dominant forms of AD. Others disagree. ‛
Autopsy studies suggest that neurofibrillary tangles first appear in the locus coeruleus (LC) of the brainstem. Now, a longitudinal imaging study lends support to that theory. LC degeneration on MRI, a proxy for tangles, precedes tau PET positivity in the medial temporal lobe, and poor cognition, by three years.
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