By injecting tau-enriched extracts derived from AD brains into transgenic mice, researchers dissect how Aβ plaques fuel tau pathology.
Slow vital capacity, a measure of respiratory function, predicted the rate of disease progression in ALS patients, suggesting the test could be used as a primary endpoint in clinical trials.
Small molecules that stabilize G-quadruplexes cut C9ORF72 RNA and protein deposits in half.
A segment of tau forms a tight molecular zipper that promotes fibrillogenesis. Zipper inhibitors blocked aggregation of full-length tau in cells.
Plaque fibrils differ markedly from person to person, yet commonalities exist among people with clinical subtypes of the disease.
A case study describes amyloidosis in a 39-year-old homozygous for a TREM2 mutation, but experts question the interpretation.
TIA1 bolsters tau toxicity, leading to synaptic malfunctions, cognitive impairment, and early death in transgenic animals.
Amyloid predicts general cognitive decline, while hippocampal shrinkage heralds only memory loss.
A 24-year prospective study links high levels of systemic inflammation markers in middle age to memory and loss of brain volume, including areas associated with Alzheimer’s disease.
The neurodegeneration marker appears to track disease severity in AD and MS patients with great sensitivity.
In people with ALS, researchers identified 39 new genetic variations in RNA-binding proteins that may influence the disease. Such information could inform future pharmacogenomics treatment.
New fluorescent tracers reveal cerebrospinal fluid leaving the skull through lymph vessels that run close to cranial nerve sheaths. This slows with age.
The philanthropist today announced a $50 million investment in the U.K.’s Dementia Discovery Fund, which supports startups developing innovative treatments.
Wild-type mice exposed to blood from Alzheimer’s amyloidosis mice developed plaques, tau phosphorylation, neuroinflammation, and synaptic deficits.
Signals from neuron EphB1 receptors boost neuroprotective functions in astrocytes. This line of communication appears cut in ALS.