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Filaments of Aβ42 struck different poses in people with sporadic versus familial AD. The familial AD structure was also found in people with other neurodegenerative diseases, and even in APP knock-in mice.
The largest transcriptomic catalogue of live microglial cells to date, MiGA cinched causal connections between genetic variation, microglial gene expression, and disease.
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.
Cerebrospinal fluid p-tau217 and -181 rose in tandem with amyloid deposition in the brain, regardless of whether the plaques contained Aβ or amyloid formed by a different protein.
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?
Well-known to the Alzheimer’s community, John Hardy is being recognized with the knighthood in the U.K’s New Year Honours.
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.
Funding will support risk factor research and public health messaging about lifestyle modifications.
Tau PET holds a slight edge over the plasma marker in people who already have mild cognitive impairment.
Without TREM2, microglia remained trapped in a homeostatic state and failed to clear TDP-43 aggregates. In a surprising twist, the two proteins were found to interact.
Shooting synaptosomes through a mass spectrometer, scientists found that those with high CD47 and low ApoE were resilient in AD brain.
Tissues from old people, both healthy and diseased, overexpress genes lacking C-G repeats. This stokes inflammation, possibly explaining why neurodegeneration rises with age.
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.
Parkinson’s mice that got deeper slow-wave sleep cleared synuclein deposits, perhaps via better glymphatic function. Sleep deprivation worsened synuclein phosphorylation and aggregation.
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?
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