Motor Neuron Vulnerability: The Case of the Missing Chaperone?
Motor neurons may be susceptible to ALS because they lack a chaperone that folds SOD1.
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Motor neurons may be susceptible to ALS because they lack a chaperone that folds SOD1.
Researchers found inherited recessive or dominant de novo mutations in people with sporadic ALS whose parents did not have the disease.
Antibody against aggregated Aβ reported to clear out amyloid from brain, and perhaps slow cognitive decline, in people with prodromal Alzheimer’s disease.
Sequences of more than 2,600 Icelanders link loss-of-function mutations in the ABCA7 gene to increased risk for Alzheimer’s.
Approximately 4 percent of familial ALS cases may be due to TBK1 mutations.
A novel assay detected two strains of human SOD1 in mice expressing the protein. They differed from those that formed in vitro. Researchers hope to use the technique to identify strains of other problem proteins as well.
Microbleeds in the brain portend either stroke or cardiovascular events, depending on where they occur.
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The newest contender in the race for a drug to rein in the β-secretase enzyme debuted with data that reflected a methodical approach to understand a drug’s performance in cerebrospinal fluid before looking for efficacy.
Epigenetic changes in the C9ORF72 promoter do not prevent disease, but they do decelerate brain atrophy and memory loss.
Two new open-access journals will cover specialized areas of Alzheimer’s research.
A screen in round worms identifies a novel mechanism for degradation of toxic proteins.
Qualification could follow, but only if trial sponsors fork over fresh data.
By dampening translation, these tiny RNAs keep protein levels from fluctuating wildly.