In induced human microglia, the E4 allele profoundly affected their health and cellular responses, while familial Alzheimer’s mutations had little effect.
Biogen and Eisai announced the discontinuation of the Phase 3 program. Elenbecestat was the only remaining BACE inhibitor being tested for AD.
The Phase 2 study missed its primary endpoint. While fewer developed dementia in the treatment group, the effect was not statistically significant. People on drug had less brain atrophy than those on placebo.
New data strengthen the idea that a healthy locus coeruleus keeps memory sharp into old age.
The organelles express unique sets of proteins depending on their environment. Astrocyte mitochondria process lipids better than those in neurons.
The pattern varied from person to person, depending on the site of injury, in contrast to the stereotyped distribution of tau tangles seen in Alzheimer’s disease.
In patient-derived neurons, tau mutations scupper lysosomes and SORLA shunts APP through different types of endosomes.
The protein forms cohesive rafts along microtubules, protecting them from digestion and regulating movement of molecular motors.
Virtual Exhibit Hall
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome F. Hoffmann-La Roche, joining our other exhibitors — Biogen, BioLegend, Dash Genomics, Inc., Abcam, BrainXell, and the Jackson Laboratory.
Mitochondria aren’t all created equal. A new study suggests that the organelles marshal cell-specific proteomes and carry out cell-specific functions. Initial findings from “MitoTag” mice identify mitochondrial proteins unique to different neuronal subtypes and to glia. These markers seem scarce around Aβ plaques and in the spinal cords from ALS patients. MitoTag mice may facilitate studies of mitochondrial dysfunction in neurodegenerative diseases.
Tau undergoes liquid-liquid phase separation to form droplets in solution. New data suggests that a similar condensation occurs along microtubules, where tau self-associates to wrap around stretches of the filaments. These dense tau islands impede some molecular motors that trundle up and down microtubules, but allow others to pass. The islands also protect against two enzymes notorious for severing microtubules. The results suggest condensation is part of tau’s normal, everyday function.
- Jason Ulrich on Among AD Mutations, Only ApoE4 Seems to Hobble Microglia
- Julia TCW on Among AD Mutations, Only ApoE4 Seems to Hobble Microglia
- Scott Counts on Tiny Brain Structure Plays Big Role in Memory
- Russell Swerdlow on Hello Mitochondriomics: Tagging Method Identifies Different Subtypes
- Mark Cookson on Hello Mitochondriomics: Tagging Method Identifies Different Subtypes
- Maria Ankarcrona on Hello Mitochondriomics: Tagging Method Identifies Different Subtypes
- Gil Rabinovici on PET Identifies Tangles Decades after a Single Traumatic Brain Injury
- Benjamin Wolozin on Islands of Tau Coat and Protect Cytoskeleton
- Kenneth Kosik on Islands of Tau Coat and Protect Cytoskeleton
- Jürgen Götz on Islands of Tau Coat and Protect Cytoskeleton
- Marco Colonna and Simone Brioschi on Are Microglia Plaque Factories?
- Mathias Jucker on Are Microglia Plaque Factories?
- Christian Haass and Samira Parhizkar on Are Microglia Plaque Factories?
- John Breitner on In Alzheimer’s, More TREM2 Is Good for You
- Alberto Lleó on Familial AD Mutations, β-CTF, Spell Trouble for Endosomes
- Christian Haass and Michael Ewers on In Alzheimer’s, More TREM2 Is Good for You
- Keenan Walker on Blood Pressure: How Low to Prevent Dementia—and When?
- David Hansen on In Alzheimer’s, More TREM2 Is Good for You
- Gary Landreth on In Alzheimer’s, More TREM2 Is Good for You
- Victor Bustos on Familial AD Mutations, β-CTF, Spell Trouble for Endosomes
- David Knopman on Blood Pressure: How Low to Prevent Dementia—and When?