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.
The agency’s request for information seeks feedback on the nature and value of the prize. Help shape it!
A longitudinal study identified regions in the default mode network as among the first to accumulate Aβ.
A crystal structure of the kinase bound to its substrate ubiquitin reveals role of unique PINK1 domains in phosphorylation and explains why certain mutations cause Parkinsonism.
Neuronal plasticity falters with Alzheimer’s disease, but noninvasive stimulation strengthens it. Meanwhile, mini-jolts inside the brain improve face recognition in epilepsy patients.
Participants in the A4 prevention trial wanted to know the extent of their amyloid burdens and how that affected their risk for AD. Researchers need to carefully communicate the limitations of amyloid PET.
The scheme catches earlier cases of Aβ accumulation than do global amyloid PET measures with binary positivity thresholds. And: the neuropathologists were right.
In motor neurons carrying familial ALS FUS mutations, axonal transport of mitochondria stalls. HDAC6 inhibitors get traffic flowing again.
The peptides may activate Nogo receptor signaling to block assembly of new synapses and compromise learning.
By harnessing a CRISPR-Cas nuclease that targets RNA, scientists have developed a way to edit transcripts, paving the way for RNA editing in mammalian cells.
Researchers debut a statistical model that uses MRI, CSF, and demographic data to compute a cognitively impaired person’s risk for progressing to dementia.
Using a new algorithm that measures mRNA decay rates more accurately than before, scientists claim that two RNA-binding proteins and four miRNAs determine the stability of mRNAs in the brain. Loss of RBFOX1 may destabilize synaptic protein mRNAs in Alzheimer’s disease.
A single-nucleotide polymorphism near the TMEM106b locus boosts expression of the gene, which is linked to frontotemporal dementia.