The amyloid imaging agent florbetapir predicts cognitive decline much like its forerunner, PiB
Low levels of 10 phospholipids in blood plasma correlated with future cognitive decline in older adults, hinting at diagnostic potential.
Scientists may have discovered another explanation for why DNA repeat sequences cause neurodegenerative diseases: A six-nucleotide expansion in the C9ORF72 gene forms stable structures that interfere with its transcription.
The scientific spotlight often shines on excitatory neurons as the brain’s main Aβ factories. What about other cell types?
The first longitudinal data from DIAN conflict with some cross-sectional findings, revealing a small drop in CSF injury markers after the first appearance of symptoms of disease.
AstraZeneca’s BACE inhibitor AZD3293 moves forward to a Phase 2/3 trial, joining Merck’s MK-8931 as the most advanced current compounds in this class.
Superficial siderosis, a leakage of blood matter onto the outer surface of the cerebral cortex, may be linked to AD and other dementias.
In Fragile X syndrome, mRNA from the mutant FMR1 gene binds to its own DNA to suppress protein expression. Could the same thing happen in other repeat expansion diseases?
The widespread damage that results from a hexanucleotide repeat expansion in the C9ORF72 gene arises from yet another oddity in the DNA’s structure, according to a new study. Rich in guanine, the long repeats on the sense strand of DNA cause it to fold up tight on itself, leaving the opposite strand exposed. The complementary sequence on the gene's own mRNA then binds the antisense DNA. The RNA-DNA hybrid halts transcription in midstream, leaving incomplete RNA fragments that pile up and trap essential proteins. Scientists think a similar mechanism may be at work in other repeat-expansion diseases.
- Cara Westmark on Genetic Suppression of Transgenic APP Rescues Hypersynchronous Network Activity in a Mouse Model of Alzeimer's Disease.
- Roberto Malinow on Florbetapir F 18 amyloid PET and 36-month cognitive decline:a prospective multicenter study.
- Lucia Huntington on Florbetapir F 18 amyloid PET and 36-month cognitive decline:a prospective multicenter study.
- David Knopman on Amyvid Follows in PiB’s Footsteps
- Huntington Potter on A role for sorting nexin 27 in AMPA receptor trafficking.
- David Holtzman on Neuronal activity regulates extracellular tau in vivo.
- Irene Griswold-Prenner on Neuronal activity regulates extracellular tau in vivo.