The first high-resolution structures of tau filaments isolated directly from an Alzheimer’s brain lay bare C-shaped protofilaments with a surprising twist.
Microglia lacking TDP-43 efficiently remove Aβ. In the process, they go a little crazy and also attack and destroy synapses.
A U.S. study claims that proton pump inhibitors commonly used to treat acid reflux are not associated with an increased risk of dementia, countering a recent German study.
Biopsies from kids with stomach distress reveal nerve cells that release α-synuclein during infection.
In older carriers of the Alzheimer’s risk allele, certain brain regions fail to adapt to increasing task difficulty.
Aberrant proteins made in C9ORF72 cells disrupt splicing by binding U2 snRNP, a key component of the spliceosome.
Researchers combine seven factors to predict if PD patients will become demented in the decade after diagnosis.
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.
In tau knockout mice, brain insulin signaling fizzled, resulting in synaptic deficits and problems with peripheral metabolism. Could this pathway be at work in Alzheimer’s?
By accounting for harmless variants of known ALS genes, researchers made a downward correction of the genetic risk associated with sporadic cases.
CHCHD10 mutations target mitochondria and TDP-43, while a UBQLN4 allele hits the proteasome.
A review of the latest data hints that blood pressure control, exercise, and cognitive training may preserve memory. But scientists require more convincing before they’ll make concrete recommendations.
The QC enzyme inhibitor reduces production of pyroglutamate Aβ, a particularly toxic, sticky form.
White blood cells from certain Parkinson’s patients react to α-synuclein peptides. Is this autoimmune reaction why the major histocompatibility complex is genetically linked to the disease?
The discovery hints that microglia, rather than neurons, may control much of a person’s genetic susceptibility to Alzheimer’s disease.