Second Study Salutes TANK-Binding Kinase 1 as ALS Gene
Approximately 4 percent of familial ALS cases may be due to TBK1 mutations.
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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.
Biogen Antibody Buoyed by Phase 1 Data and Hungry Investors Antibody Against α-Synuclein Looks Safe In Phase 1 At AD/PD Meeting, New BACE Inhibitor Struts Its Stuff D-peptides as Drugs? Protein Therapy Approaching Phase 1 Trials New Genetics Frontiers: Fi
Treatments targeting the main pathological protein of Parkinson’s disease are moving toward the clinic, with two immunotherapies passing Phase 1 safety benchmarks.
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.
The highs and lows of cerebrospinal fluid Aβ and PET amyloid imaging don't necessarily agree.
Peptides made from D-amino acids bind to Aβ oligomers and trigger their removal from the brain. Some appear poised to enter Phase 1.
At the AD/PD conference, researchers reported a protective gene variant that delays Alzheimer’s onset by 10 years, and parsed pathways to find out why particular neurons take the hit in specific diseases.
New data argue that multimers of α-synuclein may protect against pathological aggregation.
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