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.
Researchers who packed the lecture halls for “Common Mechanisms of Neurodegeneration” and “Microglia in the Brain,” joint Keystone Symposia held June 12-16 in Keystone, Colorado, saw old dogmas fall and new ideas and methodologies emerge. Debates ran the gamut from the biophysical nature of toxic proteins to the characterization of microglia in health and disease. Read Tom Fagan’s overview, then check back in the coming weeks as we bring detailed reports.
- Joe Verghese on Microbleeds in the Brain Portend Dementia
- Tim Bartels and Ulf Dettmer on A Sinister Side to α-Synuclein—Blocking Mitochondrial Protein Import
- Ronald DeMattos on Blood NfL Looks Good as Progression and Outcome Marker
- David Holtzman on Blood NfL Looks Good as Progression and Outcome Marker
- Tsuneya Ikezu on Ushers of Propagation? More Evidence that Chaperones Evict Disease-Associated Proteins
- Scott Small on Reelin-immunoreactive neurons in entorhinal cortex layer II selectively express intracellular amyloid in early Alzheimer's disease.
- Wataru Araki on Lodged in Late Endosomes, Presenilin 2 Churns Out Intraneuronal Aβ
- Takaomi Saido on Lodged in Late Endosomes, Presenilin 2 Churns Out Intraneuronal Aβ
- Rudy Tanzi on Lodged in Late Endosomes, Presenilin 2 Churns Out Intraneuronal Aβ
- Natura Myeku on Can’t Degrade That Pesky Misfolded Protein? Push It Off the MAPS
- Patrik Brundin on Can’t Degrade That Pesky Misfolded Protein? Push It Off the MAPS