CRISPR Verifies Risk Alleles, Improves Gene Editing
The gene-editing technology helps validate risk factors of disease and build better disease models.
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The gene-editing technology helps validate risk factors of disease and build better disease models.
Aβ Oligomers Purified from Human Brain Microbial Hypotheses Intrigue at Zilkha Alzheimer’s Meeting What’s Up With the Vasculature in Dementia? At the third annual Zilkha Symposium, held April 15, 2016, in Los Angeles, scientists from the United States and
After years of doubt, leading scientists are growing cautiously excited about the idea that bacteria might seed plaques.
Zilkha conference features news on tau toxicity, a leaky blood-brain barrier, and the biology of pericytes.
Nuances in episodic memory can tell if primary progressive aphasia is due to non-tangle types of tau pathology or to plaques and tangles.
Age-related attrition of the male chromosome in blood cells raises the risk of Alzheimer’s disease. Researchers suspect immune cells are compromised.
Mice lacking the receptor have more diffuse plaques, more dystrophic axons, and more neurodegeneration. The TREM2-microglia hail from inside the brain.
A study reports that even while young transgenic mice learn just fine, both their memory consolidation and brain glucose metabolism falter before the onset of amyloid plaques.
The kinase triggers a death cascade in animal models featuring endoplasmic reticulum stress. Active in ALS patients, it warrants a look as a potential therapeutic target.
Beginning in July, a massive open online course will summarize research on how to maximize brain health.
A dynamic joint meeting dispels some old tenets while charting new avenues for research, such as microglia from iPSCs.
Keystone Meeting on Microglia/Neurodegeneration: Here’s the Buzz Induced Microglia Make Debut at Keystone Symposium The THIK and Thin of Microglial Surveillance When a Microglia Is No Longer a Microglia Unbiased Screen Fingers TREM2 Ligands That Promote A
Three research groups turn induced pluripotent stem cells into what look like microglia.
Loose in the cytoplasm, TDP-43 heads straight for the neuronal powerhouses, sapping their ability to make energy.
Seeking strength in numbers, families gathered to swap stories and to learn about an upcoming DIAN-TU therapy trial geared specifically to their particular form of early onset AD.