NIA Seeks Community Input on Alzheimer’s Eureka Prize
The agency’s request for information seeks feedback on the nature and value of the prize. Help shape it!
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The agency’s request for information seeks feedback on the nature and value of the prize. Help shape it!
Souvenaid missed its primary cognitive endpoint in the two-year trial, but reduced brain atrophy and slowed functional decline.
Tau fibrils isolated from people with AD, PSP, and CBD recapitulated the typical pathology of each disease in animals without human transgene expression.
Expressed in the brains of mice, a secreted form of the anti-aging protein, klotho, protects from an age-related decline in memory.
Signals from neuron EphB1 receptors boost neuroprotective functions in astrocytes. This line of communication appears cut in ALS.
Wild-type mice exposed to blood from Alzheimer’s amyloidosis mice developed plaques, tau phosphorylation, neuroinflammation, and synaptic deficits.
The philanthropist today announced a $50 million investment in the U.K.’s Dementia Discovery Fund, which supports startups developing innovative treatments.
New fluorescent tracers reveal cerebrospinal fluid leaving the skull through lymph vessels that run close to cranial nerve sheaths. This slows with age.
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.
The neurodegeneration marker appears to track disease severity in AD and MS patients with great sensitivity.
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.
Amyloid predicts general cognitive decline, while hippocampal shrinkage heralds only memory loss.
TIA1 bolsters tau toxicity, leading to synaptic malfunctions, cognitive impairment, and early death in transgenic animals.
A case study describes amyloidosis in a 39-year-old homozygous for a TREM2 mutation, but experts question the interpretation.
Plaque fibrils differ markedly from person to person, yet commonalities exist among people with clinical subtypes of the disease.
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