PET study finds tau signal associated with markers of cerebrovascular disease and cognitive issues.
Not the brown trucks with the friendly delivery guys, the unconventional protein secretion pathway. Tau rides it to slink out of one cell, and, grabbing onto heparin sulfate proteoglycans, enter another and stoke aggregation there.
Company has halted all trials of atabecestat.
Engineered nanoparticles snatched extracellular Aβ, ferried it into cells, and switched on autophagy, clearing the peptide from the brains of mice. Would this work as a drug?
Contrary to previous findings, both proteins seem to escape via passive diffusion. This has implications for therapeutic strategies to keep them where they belong.
Aggregates that form inside, or just pass through, oligodendrocytes take on the properties of the virulent strain that gives rise to multiple system atrophy.
ApoE4 raises CSF tau more in women than in men, suggesting sex may influence the risk of neurodegeneration, especially in amyloid-positive E4 carriers.
Exposure to lipid membranes embedded with cholesterol accelerate Aβ fibril formation by up to 20-fold.
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Amyloid, tau, and vascular pathology often co-exist. The first PET study of tau tracer uptake in people with well-defined cerebrovascular disease finds increased AV1451 uptake occurs independently of concurrent amyloid pathology. Tau signal in the inferior temporal cortex correlates with vascular disease load and cognitive decline.
Why do different strains of the same prion-like protein occur in different diseases? New research suggests a surprising answer: The cell type is to blame. Researchers claim that aggregates of α-synuclein that form in, or even pass through, oligodendrocytes take on more toxic properties than strains found in neurons. The findings may explain why multiple system atrophy, which is characterized by glial deposits of α-synuclein, progresses more rapidly than Parkinson’s disease.
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- Wilfried Rossoll on No, TDP-43 and FUS Are Not Actively Exported From the Nucleus
- Ke Zhang on No, TDP-43 and FUS Are Not Actively Exported From the Nucleus
- Sami Barmada on No, TDP-43 and FUS Are Not Actively Exported From the Nucleus
- Mike Miguel Pappolla on Cholesterol Greases the Aβ Aggregation Machine
- Rena Li on Study Finds Sex Influences CSF Tau Levels in ApoE4 Carriers
- Christian Pike on Study Finds Sex Influences CSF Tau Levels in ApoE4 Carriers
- Tobias Hartmann on Cholesterol Greases the Aβ Aggregation Machine
- Elaine R Peskind on Do Mild Traumatic Brain Injuries Double the Risk of Dementia?
- Michelle Mielke on Do Mild Traumatic Brain Injuries Double the Risk of Dementia?
- Steven DeKosky on Do Mild Traumatic Brain Injuries Double the Risk of Dementia?
- Todd E. Golde on A Little Amyloid, A Lot of Trouble?
- Yoshihide Esaki on Japanese ADNI Data Parallel North American ADNI, Encouraging Global Trials
- Howard Feldman on Japanese ADNI Data Parallel North American ADNI, Encouraging Global Trials
- Terrence Town on Loss of Soothing Lipids in AD Brain Furthers Microglial Mayhem
- Val Lowe on A Little Amyloid, A Lot of Trouble?
- Victor L. Villemagne and Colin Masters on A Little Amyloid, A Lot of Trouble?
- Keith Johnson on Move Over, Flortaucipir? New Tau Tracers Tested in People
- Jeffery Kelly on Small Molecule Keeps Mutant SOD1 Out of Trouble
- Kristine Freude on In Mice, CRISPR-Based Alzheimer’s Therapies Inch Forward
- Randall Bateman on ABBY: A phase 2 randomized trial of crenezumab in mild to moderate Alzheimer disease.