In a human cell model, VCP variants trigger a cascade of neuronal disruption and hobble astrocytes’ ability to support motoneurons.
Mutations in certain E. coli genes extend the lives of both normal and Aβ-laden roundworms.
Tomlinson was the first to quantify plaques and tangles in the postmortem brain, launching the modern era of Alzheimer’s research.
New diagnostic guidelines on dementia with Lewy bodies fold in science about sleep and the heart, two aspects that distinguish this disorder from Alzheimer’s and Parkinson’s.
Study of A673T carriers strengthens case for reducing Aβ to prevent AD.
Longitudinal ADNI data revealed that people with elevated Aβ declined toward AD, while those with normal levels maintained their cognitive abilities.
A study suggests DJ-1 may protect against oxidative stress by trimming unwanted sugar modifications from biomolecules.
The protease cleaves three C-terminal fragments of the amyloid precursor protein at different amino acid positions.
The transcriptomes of single immune cells in the mouse brain identify specific disease-associated microglia (DAM), which eat away at Aβ deposits.
An unbiased analysis of positron emission tomography data traces long-distance connections between amyloid and tau pathology in the cortex.
Scientists lay out the first combined epigenomic and transcriptional profile of human microglia. The signature is similar to that of mice, but quickly vanishes when cells are placed in a dish.
At the length that triggers disease, expanded nucleotide repeats cause RNAs to clump into semi-solid foci.
Without the C3 protein, microglia calm down and the mice preserve their memories.
A phosphorylated version of the protease ramps up autophagy, promoting degradation of the C-terminal fragment of amyloid precursor protein, the source of Aβ.
Injected α-synuclein fibrils triggered pathology throughout the mouse brain, even in regions not neuroanatomically connected to the injection site. Astrocytes were loaded with inclusions.