Mice with amyloid plaques develop runaway neuroinflammation, whereas mice with tau tangles predominantly lose synapses, a gene-expression study reports.
The addition of a sugar to β-secretase ramps up Aβ production. Could reducing that sweet addition slow progression of Alzheimer's?
Neurons derived from stem cells of people with amyotrophic lateral sclerosis bungle the transmission of electrical signals.
Irritability and depression emerge sooner in AD than in the general population.
Both motor neurons in the brain and neuromuscular junctions in the periphery exhibit defects in young ALS mouse models.
High levels foreshadow cognitive loss, hinting at utility as early diagnostic biomarkers.
Using baseline brain scans, the model projects where atrophy will occur and metabolism will wane.
A protein that repairs synapses after hibernation falters in some models of neurodegenerative diseases.
How do the hallmark pathologies of Alzheimer's contribute to disease? According to a new gene-expression analysis of different mouse models, Aβ plaques trigger neuroinflammation but spare synapses, whereas tau tangles lead to synapse loss and degeneration. The results match findings from human studies, and highlight genes that may play crucial roles in each process. The publicly available dataset provides a resource for other researchers.
One small tweak to a sugar side chain on BACE1 could make all the difference when it comes to Aβ processing, scientists claim. An added monosaccharide appears to slow BACE1’s trek toward the lysosome, keeping it around longer to cut amyloid precursor protein. APP transgenic mice that grew up without the enzyme responsible for this step developed less pathology. Could it provide a new drug target for Alzheimer’s?
- Frances Edwards on A genome-wide gene-expression analysis and database in transgenic mice during development of amyloid or tau pathology
- Gerold Schmitt-Ulms on A genome-wide gene-expression analysis and database in transgenic mice during development of amyloid or tau pathology
- Riqiang Yan on An aberrant sugar modification of BACE1 blocks its lysosomal targeting in Alzheimer's disease.
- Soraia Barao and Bart De Strooper on An aberrant sugar modification of BACE1 blocks its lysosomal targeting in Alzheimer's disease.
- Shi-Yan Ng on Human iPSC-derived motoneurons harbouring TARDBP or C9ORF72 ALS mutations are dysfunctional despite maintaining viability.
- Angeliki Nikolakopoulou, Anita Ramanathan, Amy Nelson and Berislav Zlokovic on Aging-induced type I interferon response at the choroid plexus negatively affects brain function.
- Gael Chetelat on Associations Between Biomarkers and Age in the Presenilin 1 E280A Autosomal Dominant Alzheimer Disease Kindred: A Cross-sectional Study.