Stimulating mouse neurons makes them pump out, and take up, more aberrant tau, intensifying its aggregation and possibly facilitating pathological spread.
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 dynamic joint meeting dispels some old tenets while charting new avenues for research, such as microglia from iPSCs.
The co-chaperone DnaJC5 teams up with Hsc70 to guide potentially toxic proteins out of neurons. Whether this facilitates transcellular propagation remains to be seen.
Beginning in July, a massive open online course will summarize research on how to maximize brain health.
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.
Not exosome, not proteasome, not autophagy: Could a new pathway dubbed MAPS facilitate the spread of amyloidogenic proteins?
Large longitudinal study links tiny hemorrhages in cerebral capillaries to lower cognitive test scores, higher risk of dementia.
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.
Oligomers block outer membrane translocases, starving the organelles of essential respiratory chain components.
In a large affected family, mutation of a transmembrane protein implicates defective cellular recycling in the disease.
Presenilin 2 resides almost exclusively in late endosomes, multivesicular bodies, and lysosomes, where it generates a pool of aggregation-prone Aβ. Some PS-1 mutations phenocopy this intraneuronal distribution.
Levels of neurofilament light in blood and spinal fluid of mice reflected brain pathology and changed with treatment.
A bill approved by the U.S. Senate Appropriations Committee would increase funding for Alzheimer’s and related dementias by 40 percent.
The misfolded miscreants interact with their normal brethren on the neuronal surface to trigger the damage, but how and whether this collapse relates to prion propagation remains a mystery.
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