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.
Expressed in the brains of mice, a secreted form of the anti-aging protein, klotho, protects from an age-related decline in memory.
Tau fibrils isolated from people with AD, PSP, and CBD recapitulated the typical pathology of each disease in animals without human transgene expression.
Souvenaid missed its primary cognitive endpoint in the two-year trial, but reduced brain atrophy and slowed functional decline.
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A longitudinal study identified regions in the default mode network as among the first to accumulate Aβ.