Should People on Blood Thinners Forego Leqembi?
Recent reports of three deaths in the lecanemab extension study suggest that blood thinners, lecanemab, and cerebral amyloid angiopathy could be a dangerous combination.
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2022 Was Good to Basic Research, Too
Last year saw major advances in multi-omics analyses using human tissues, better animal models, deeper functional studies of gene variants, dissections of neuroimmune cell biology, and more.
Neuroinflammation Field Grapples With Complexity at Keystone Symposia
Researchers explored how the brain’s immune cells influence disease, and how cells and signals from outside the brain pitch in.
Just Like Viruses, Tau Can Unleash Interferons
By triggering release of mitochondrial DNA, tau fibrils may set off a cytosolic sensor that activates the interferon response. Blocking this sensor spared neurons and memory in mice.
In Progressive Supranuclear Palsy, Filamin-A Goads Tau Aggregation
The actin-binding protein associated with tau aggregates in people with PSP, and rare variants in the gene associated with the disease.
2022, a Year in Review
Therapeutics research in the field ended on high hopes that lecanemab’s Phase 3 data would carry this anti-Aβ antibody to regulatory approval in country after country in 2023. This wave drew power from progress in biomarker research; but alas, much work remains to be done.
Death by Goo: TDP-43 Gels Paralyze Proteasomes in Neurons
Cryo-electron tomography reveals amorphous blobs of TDP-43 C-terminal fragments. They ensnare stalled proteasomes in the cytosol.
How TDP-43’s Disheveled Tail Spells Trouble
Atomic-level analysis of the protein’s C-terminal end suggests a floppy region key for the delicate process of forming functional oligomers. Mutate it slightly, and it becomes an aggregating machine.
Stress Granules: No Incubator for Inclusions, After All?
Using a new optogenetic model for TDP-43 phase transitions, scientists see the protein aggregate outside, not inside stress granules. The model distinguishes physiological from abnormal phase transition.
Differential Diagnosis: Can Synaptic Proteins Get It Done?
VAMP2 helps distinguish pure dementia with Lewy bodies from DLB with Alzheimer’s. A synaptic protein panel distinguished FTLD-TDP-43 from FTLD-tau.
Up, and Down—Haptoglobin Moves APOE4 Risk in Mysterious Ways
The blood protein tempers APOE4 risk in E2 carriers yet accentuates it in E4 homozygote people.
Eavesdropping on Cell-to-Cell Conversations in Aging, Alzheimer's
New, unbiased single-cell methods uncover coordinated changes in cell populations and their interactions. These correlate with disease pathology, progression.
Could Juicing Up Trafficking Abolish ApoE4’s Alzheimer’s Risk?
In an amyloidosis mouse, inhibiting the endosomal proton leak channel NHE6 sped up recycling of ApoE. This slashed amyloid deposition and restored synaptic plasticity.
Paper Alert: Plasma P-tau217 Predicts Future Cognitive Decline
Cognitively normal older adults with high levels of the biomarker slid quickly toward dementia.
Emerging Alzheimer’s Therapies Test the Waters at CTAD
A few attempts at Alzheimer’s therapy claim hints of promise in early clinical trials, though several did not include placebo controls.
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