Bloodborne Tau: Foggy Window into the Brain for TBI, Dementia
Tau in the plasma rises after traumatic brain injury, with cognitive decline, and progression to mild cognitive impairment.
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Tau in the plasma rises after traumatic brain injury, with cognitive decline, and progression to mild cognitive impairment.
The RNA-binding protein FUS promotes synthesis of an isoform of SynGAP, a protein that bolsters dendritic spines. Restoring SynGAP expression partially rescued deficits in FUS–deficient mice.
New CRISPR screen flags dozens of genes that suppress toxicity of the Parkinson’s protein. Tweaking multiple genes strengthened the protection.
Relatives of patients who have ALS are more likely to live with neuropsychiatric diseases such as schizophrenia, obsessive-compulsive disorder, and alcoholism.
In a massive project analyzing gene expression patterns among 44 human tissues from 449 people, researchers correlated genetic variation with region-specific transcriptomes.
A single-nucleotide polymorphism near the TMEM106b locus boosts expression of the gene, which is linked to frontotemporal dementia.
Neuronal plasticity falters with Alzheimer’s disease, but noninvasive stimulation strengthens it. Meanwhile, mini-jolts inside the brain improve face recognition in epilepsy patients.
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.
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.
The philanthropist today announced a $50 million investment in the U.K.’s Dementia Discovery Fund, which supports startups developing innovative treatments.
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.
A case study describes amyloidosis in a 39-year-old homozygous for a TREM2 mutation, but experts question the interpretation.
Small molecules that stabilize G-quadruplexes cut C9ORF72 RNA and protein deposits in half.