Paper Alert: TREM2 Crucial for Microglial Activation
Immune cells lacking the receptor fail to respond to injury and aging, resulting in overall poor brain health in mouse models.
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Immune cells lacking the receptor fail to respond to injury and aging, resulting in overall poor brain health in mouse models.
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.
In a human cell model, VCP variants trigger a cascade of neuronal disruption and hobble astrocytes’ ability to support motoneurons.
CHCHD10 mutations target mitochondria and TDP-43, while a UBQLN4 allele hits the proteasome.
By accounting for harmless variants of known ALS genes, researchers made a downward correction of the genetic risk associated with sporadic cases.
Based on the tiny effect size seen in overall negative solanezumab trials in mild Alzheimer’s disease, researchers are going big in a secondary prevention trial.
Instead of clearing plaques, do microglia seed them? The brain’s immune cells continue to take researchers by surprise.
Microglial Regulation and Function Scrutinized at Heidelberg Meeting A New Explanation for Dendritic Tau: It’s Made There Alzheimer’s Proteomics Treasure Trove? sAPP Binds GABA Receptor, and More News on APP At Heidelberg meeting, scientists shared and de
23andMe sells people information about their Alzheimer’s and Parkinson’s risk. They include tricky-to-interpret raw data on dozens of disease genes. Should such direct-to-consumer testing companies offer better counselling and referral?
A new prize seeks the ideal mix of factors to forecast who will progress to Alzheimer’s symptoms.
At a conference in Heidelberg, researchers proposed that Aβ oligomers trigger local translation of tau in cytosol and dendrites, and that targeting this aberrant tau may preserve synapses.
Analysis of brain tissue from Alzheimer’s patients offers a glimpse of proteomic changes in the disease.
The prevalence of chronic traumatic encephalopathy supports a link between multiple concussions and this degenerative tauopathy, though the sample is self-selected.
An astrocytic Aβ protease, destabilization of γ-secretase by FAD mutations, and an sAPP receptor all made their debuts at Heidelberg conference.
At AAIC, researchers debuted a method that detects changes in plasma Aβ42 in people with brain amyloid. If confirmed, a widely available screening test for presymptomatic AD could follow.