A bit less strapped for funding, researchers are considering the next steps for Lewy body, frontotemporal, and vascular dementia.
AD-Related Dementias Summit 2016: Progress, Aims, Dollars At 2016 Summit, Field Tackles AD-Related Dementias One By One Did you know the U.S. National Alzheimer’s Project Act covers Lewy body, frontotemporal, vascular, and mixed dementias, as well? It ...
NAPA's latest collective exercise was a conference to update the field on progress in the past three years and advise the NIH on how to spend the next round of funds.
Neurogeneticists honored for their discoveries, especially of repeat expansions that cause ALS/FTD.
Scientists report that the transcription factor NRF2 regulates tau expression, stimulating production of a protective isoform.
A NOVA special gets up close and personal with Alzheimer’s researchers and their patients, asking if this disease can be stopped.
Alois was right: Among cognitively normal middle-aged people followed for more than a decade, memory worsened only in those in whom markers for both amyloid and tau were abnormal.
Vervet monkeys that model type 1 diabetes have early markers of Alzheimer’s in their brains, providing possible insights on the connection between the two diseases.
Thirteen “escapees” of childhood illness offer hope of finding protective variants that may pay dividends.
Study improves confidence in three core biomarkers and five emerging markers, most in cerebrospinal fluid and one in blood.
Souvenaid Trial Missed Primary, Partially Met Secondary Endpoints New Tack on Aβ Oligomer Role in Disease and Treatment The 14th International Athens/Springfield Symposium on Advances in Alzheimer Therapy was held March 9 to 12 in Athens, Greece. ...
At Athens meeting, scientists had new data on where these species appear in the brain, how they disrupt neurons, and whether oligo-specific antibodies would work.
An FDA panel recommended the drug for approval, which would make it the first antipsychotic cleared for use in a neurodegenerative disease.
The modified protein prevents the synaptic protein KIBRA from managing plasticity.
Knocking out neuronal heparan sulfate proteoglycans slashed plaque load and facilitated Aβ clearance in AD model mice.