Desikan pioneered advances in neuroimaging and neurogenetics, and was known for his passion and collaborative spirit.
Viral surfaces attract proteins from the extracellular environment of the person they infect. This corona of host proteins makes the virus more or less infective—and promotes amyloid fibrils.
In mice, the back of the brain, near the neck, contains lymphatic vessels that are specialized to take up cerebrospinal fluid and deliver it to cervical lymph nodes.
The company halted its Phase 2 trial of ABBV-8E12 due to lack of efficacy.
In response to the peptide, these little cells squeeze capillaries, constricting them. This may contribute to neuronal dysfunction.
Longitudinal data identifies four stages of amyloid plaque buildup, with the earliest deposits appearing in the precuneus and posterior cingulate.
Co-sponsors Banner, Novartis, and Amgen announced that they will stop testing CNP520 in two Phase 2/3 studies in people at risk of AD. The drug worsened cognition.
Functional variants of AD GWAS hits found in enhancers of myeloid genes.
A PLCG2 variant that reduces a person’s risk of Alzheimer’s, frontotemporal dementia, and dementia with Lewy bodies also appears to extend longevity.
Aβ deposits make distal neurons vulnerable to insults, including from local Aβ, says imaging study. The combination hastens cognitive decline.
New strains have amyloid, neurodegeneration, and neuroinflammation, all against a background of natural genetic variation.
New evidence suggests the dimers impede clearance of glutamate from synapses, contributing to the hyperexcitability seen early in Alzheimer’s disease.
The phenotype of ApoE4 astrocytes and microglia resembles that of these cells in Alzheimer’s brain. Could defects in lipid metabolism and the extracellular matrix bring on the disease?
The locus incertus fine-tunes hippocampus neural activity to control memory formation in stressful situations. Could a new understanding of these circuits shed light on memory loss in Alzheimer’s?
Serial amyloid and tau scans in cognitively healthy people indicate that the speed at which a person’s tau accumulates best predicts his or her future cognitive decline.