ALS-Linked Kinase Promotes Mitochondrial Destruction
TBK1 helps autophagy adaptors clutch damaged organelles.
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TBK1 helps autophagy adaptors clutch damaged organelles.
Neurogranin could be a promising early CSF biomarker of Alzheimer’s disease.
Gastrointestinal adverse events prompted the FDA to press the pause button on the α7 nicotinic acetylcholine receptor agonist.
The latest optical-clearing technique exposes three-dimensional interactions between plaques, microglia, and blood vessels. It even zooms in on synapses.
Mutations in CHMP2B gene have been linked to mysterious lysosomal inclusions.
Avanir Pharmaceuticals’ AVP-923 calmed Alzheimer’s patients in a small 10-week study.
The 1000 Genomes consortium released its final report and sequence data set. It will help scientists studying neurodegenerative diseases better interpret GWAS findings.
Analysis of the avagacestat trial of 2012 details the side effects that sank the drug, and the outcomes that support CSF biomarkers for prodromal Alzheimer’s disease.
Researchers report the first known enzyme that combines disaggregase and protease activity.
Granules in the nucleus and cytoplasm may owe their genesis and shape to liquefied forms of ALS-linked proteins, such as FUS and hnRNPA1.
When researchers directly convert skin cells into neurons, skipping the stem-cell step, the cells express gene signatures that reflect the age of their donors.
White-matter hyperintensities, astrocyte damage, hypoperfusion, and amyloid angiopathy draw scrutiny as factors in the complex relationship between cerebrovascular and neurodegenerative processes in dementia.
VasCog 2015—Highlights of a Conference Every so often, an intrepid reader steps forward to enlighten the community by organizing notes from a conference that few fellow Alzforum readers got to attend. This week, Donna Wilcock of the University of Kentucky
Moving toward a common standard for fluid-based Alzheimer’s diagnosis in routine clinical care, an intergovernmental metrology agency has certified a way of quantifying Aβ42.
Recent studies exemplify the burgeoning array of stem cell strategies to treat neurodegeneration, ranging from sending in supportive cells to switching out neurons.