Combination therapies may work where single drugs fall short, but testing them in AD may prove challenging.
Network analysis may explain why people with semantic dementia keep making memories even as their hippocampi degenerate.
A new test claims to detect Aβ oligomers in cerebrospinal fluid by exploiting their tendency to seed aggregation.
Researchers have found protein traces of brain damage in the blood of hockey players who sustained a concussion. Could biomarkers help decide when athletes return to their sport?
Researchers identify a transcription factor that protects neurons during normal aging but goes AWOL in Alzheimer’s brains.
Much like people with Alzheimer's, mice modelling the disease experience seizures. New research suggests that APP, and not Aβ, makes their neurons hyperexcitable.
Research suggests that the kinase Cdk5 limits formation of new memories by keeping a key synaptic receptor away from the cell surface.
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?