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.
In a massive project analyzing gene expression patterns among 44 human tissues from 449 people, researchers correlated genetic variation with region-specific transcriptomes.
Seizures in AD mice lead to cognitive changes via epigenetic suppression of calbindin-D28k.
Relatives of patients who have ALS are more likely to live with neuropsychiatric diseases such as schizophrenia, obsessive-compulsive disorder, and alcoholism.
Intestinal flora helps fight infection, inflammation, and cancer. What could this mean for neurodegeneration?
TREM2 accelerates neurodegeneration in one tauopathy model, but reduces tau pathology in another. Whether the microglial protein is good or bad may depend on stage of disease.
New CRISPR screen flags dozens of genes that suppress toxicity of the Parkinson’s protein. Tweaking multiple genes strengthened the protection.
Using modified MRI protocols, researchers were able to visualize these vessels in the dura mater of living people. The discovery challenges conventional wisdom.
Researchers claim this failed drug allows Aβ to accumulate inside cells, while small peptides cleaved from the C-terminal end of APP become trapped in membranes.
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