Gene Editing for Huntington’s Disease Shows Promise in Pigs
A single injection with CRISPR machinery suppressed mutant protein and improved gait and survival, suggesting the strategy deserves further exploration.
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In Brain With Christchurch Mutation, More ApoE3 Means Fewer Tangles
The autopsy of a woman with a the PSEN1 Paisa mutation plus a homozygous ApoE3 variant showed an unusual distribution of tau tangles. Gene-expression studies pinpointed vulnerable neurons that were spared, and riled-up microglia in tangle-ridden zones.
Whole Genome Analysis Nets New Lewy Body Dementia Gene
A deletion in the gene for a lysosomal ion channel popped out of a genomic analysis of LBD risk. So did rare structural variants in other FTD and ALS genes.
Does “Good” Cholesterol Increase Your Risk of Alzheimer’s?
Mendelian randomization identified HDL cholesterol and systolic blood pressure as modifiable risk factors.
Transcriptomics Confirm Vascular Changes in Alzheimer’s Brain
Cells of the neurovascular unit upregulate inflammation-related genes and stifle genes of the blood-brain barrier. The genes include 125 known to carry AD risk variants.
Could an RNA-Binding Protein Prevent Tau Aggregation?
When human neurons and brain organoids lack G3BP2, they contain more tau oligomers. The protein binds to tau’s microtubule-binding domain.
Does TSPO PET Measure Microglia Activation or Density?
A provocative new study suggests that unlike in mice, TSPO in people does not rise with microglial activation; instead, a higher PET signal reflects more microglia.
Finally, a Diagnostic Marker for Lewy Body Disease?
α-Synuclein seed amplification assays identify people with LBD. They may outperform clinical diagnosis, and hint that dementia with Lewy bodies might be overdiagnosed.
Does Plaque ApoE Summon Microglia to Amyloid?
In mice, microglia that sprout vascular cell adhesion molecule 1 flock to amyloid aggregates. ApoE is required.
Astrocyte Receptor Suppresses Neurotoxic Lipids, Preserves Neurons
Raising TMEM164 prevents astrocytes from releasing the toxic lipids, protecting neurons in models of Alzheimer’s and Parkinson’s.
Could a Faulty Ubiquitin Trigger Amyloid and Tau Deposits?
In human three-dimensional brain cell cultures, UBB+1 caused plaques and tangles. Silencing UBB+1 prevented spontaneous amyloid pathology caused by AD mutations.
Are Microglia Plaque Factories?
Eliminating microglia in a mouse model of amyloidosis nearly abolished parenchymal plaques, but led to a huge buildup of amyloid in cerebral blood vessels.
SUMO-Wrestling with APP?
In the January 7 PNAS, researchers from the biopharmaceutical company Scios Inc. reported that sumoylation, the covalent modification of lysine residues by small ubiquitin-like modifier (SUMO) proteins, has a dramatic impact on amyloid β production...
New Therapeutic Strategy—Mimic the ApoE Christchurch Mutation?
An antibody copying the effects of the protective ApoE variant prevents tau hyperphosphorylation in the mouse eye and brain.
Amyloid, Not Vascular Disease, May Drive White-Matter Hyperintensities
These imaging abnormalities grew the most in people with many plaques or cerebral amyloid angiopathy pathology, irrespective of cardiovascular risk.
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