As ALS Worsens, Immune Cells Multiply in the Blood
A longitudinal study suggests that distinct populations of immune cells in the blood expand as the disease progresses, while others shrink.
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A longitudinal study suggests that distinct populations of immune cells in the blood expand as the disease progresses, while others shrink.
PET scans show a tangle patch in the entorhinal cortex when people report subjective cognitive concerns.
Using modified MRI protocols, researchers were able to visualize these vessels in the dura mater of living people. The discovery challenges conventional wisdom.
Intestinal flora helps fight infection, inflammation, and cancer. What could this mean for neurodegeneration?
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.
In motor neurons carrying familial ALS FUS mutations, axonal transport of mitochondria stalls. HDAC6 inhibitors get traffic flowing again.
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.
New fluorescent tracers reveal cerebrospinal fluid leaving the skull through lymph vessels that run close to cranial nerve sheaths. This slows with age.
The neurodegeneration marker appears to track disease severity in AD and MS patients with great sensitivity.
By injecting tau-enriched extracts derived from AD brains into transgenic mice, researchers dissect how Aβ plaques fuel tau pathology.
The GWAS confirms known associations, and hints at new ones. It suggests DLB is genetically distinct from AD or PD.
Publication of negative results of Phase 3 idalopirdine trials lays to rest yet another candidate drug.
A pilot study finds that depriving people of sleep bumps up their nightly Aβ production.
Scientists elucidate a new pathway by which salt triggers adaptive immune cell responses in the gut, which harm memory without driving up blood pressure.
Three new studies agree that cellular stress favors noncanonical translation of dipeptide repeats from an intron in the C9ORF72 gene, but diverge on the exact mechanism.
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