In ALS, Do Motor Neurons Go Out with a Bang or a Whimper?
Maybe it’s not hyperexcitability, after all. Correlating electrical activity with muscle strength, scientists conclude that motor neurons become hypoexcitable just before degenerating.
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Maybe it’s not hyperexcitability, after all. Correlating electrical activity with muscle strength, scientists conclude that motor neurons become hypoexcitable just before degenerating.
An antagonist to this receptor was trounced in Phase 3 trial.
At AAT-AD/PD, scientists showed that correlated amyloid patches are an even earlier marker than brain-wide positivity, while others puzzled over why tau signals are lower in older people.
Low complexity and globular domains can promote LLPS, and phosphorylation hampers both.
A comparison of these large data sets shows that while the two forms of Alzheimer’s disease have separate triggers, they follow the same course and are much more similar than different.
The epitope that a therapeutic tau antibody targets determines whether it prevents seeding in cellular assays, raising questions about first-generation antibody trials.
After Plasma Aβ, Now Plasma P-Tau181 Shows Promise To Block Tau’s Proteopathic Spread, Antibody Must Attack its Mid-Region DIAN and ADNI Data Say Familial and Sporadic AD Converge News From the PET Front: Early Amyloid Networks and Tau Mystery Alzheimer’s
Scientists at the AAT-AD/PD conference debuted new detection methods for this biomarker, which they say distinguished healthy controls from MCI and AD.
This alternative approach to Aβ immunotherapy targets unlipidated, plaque-associated ApoE.
A new protocol robustly generates microglia-like cells from human stem cells. Disease-causing TREM2 mutations have little effect on some of their innate immune responses.
No benefit detected in double-blind trial with sham surgical controls.
Injecting 13C-labeled leucine intravenously, researchers tracked tau turnover in the human brain and cerebrospinal fluid for the first time.
In a small group of Swedish women, the fittest were nearly 90 percent less likely to develop dementia.
Kinesin mutations may disrupt organelle transport, putting motor neurons at risk.
What goes up can come down—rising tides of VILIP-1, neurogranin, and SNAP-25 ebb after onset of AD symptoms.
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