Could Targeting CD22 Restore Microglial Lysosome Trafficking?
In human microglia-like cells, soluble CD22 stalled normal breakdown of fats. Blocking sCD22 greased the system, evoking a treatment for lysosomal-storage disorders.
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In human microglia-like cells, soluble CD22 stalled normal breakdown of fats. Blocking sCD22 greased the system, evoking a treatment for lysosomal-storage disorders.
Blood from fit mice reduced neuroinflammation in inactive mice. The can-do component? Clusterin, an apolipoprotein linked to Alzheimer’s. Clusterin tamped down interferon and cytokine signaling.
A repurposing study tapped sildenafil as an Alzheimer’s drug candidate. It suppresses p-tau in cultured neurons, men who take it are less prone to AD, and a trial is planned.
For amyloidogenic proteins such as Aβ and tau, third-party proteins bearing similar sequences sway aggregation kinetics. Does this underlie cells’ selective vulnerability to amyloid?
Parkinson’s mice that got deeper slow-wave sleep cleared synuclein deposits, perhaps via better glymphatic function. Sleep deprivation worsened synuclein phosphorylation and aggregation.
The EMA's decision was expected. Biogen announced it will appeal but also halved the drug's price. The company said it plans to complete a confirmatory trial by 2026.
Tissues from old people, both healthy and diseased, overexpress genes lacking C-G repeats. This stokes inflammation, possibly explaining why neurodegeneration rises with age.
Tau PET holds a slight edge over the plasma marker in people who already have mild cognitive impairment.
Funding will support risk factor research and public health messaging about lifestyle modifications.
AAV-based CRISPR snipped a piece of mutant APP and limited plaques in mice. Viruses that infiltrate only the CNS—and only neurons there—may facilitate localized gene editing in the brain.
People with subjective or mild cognitive impairment are less likely to get dementia if their CSF Aβ38 levels are high. Should γ-secretase modulators be revived?
A new study claims that diverse palettes of tau species exist in the hippocampi of people with AD. Four-repeat isoforms dominated in rapidly progressing disease.
The largest transcriptomic catalogue of live microglial cells to date, MiGA cinched causal connections between genetic variation, microglial gene expression, and disease.
Progranulin deficiency hyperactivates microglia, but calming these cells worsened synapse loss and neurodegeneration in mice.
Alzforum editors review the highlights of last year’s clinical and research developments.
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