This past year, therapeutic antibodies massively reduced brain amyloid, blood tests came into their own, and systems-based approaches transformed the study of gene expression, glial cells, and selective vulnerability.
New potential immunotherapies and insight into single-cell responses were highlights of a small meeting in Denmark.
Researchers gain traction in the study of these rare tau disorders, which are sometimes confused with Alzheimer’s disease.
Antisense Oligonucleotides: Can They Take on ALS, SMA, Prions? Drug Reported to Help Alzheimer’s Patients Sleep Better American Academy of Neurology 2019 Annual Meeting ...
By aging cultured neurons and manipulating them to stimulate endocytosis or interfere with vesicle release, researchers can bring about characteristics of Alzheimer’s—without adding APP or Aβ.
The Food and Drug Administration has said it will accept cognition alone as the basis for approval in preclinical AD. Now what? Industry is confronting the challenge to show robust and meaningful change.
Data on ASOs, presented recently at the annual meeting of the American Academy of Neurology, depict RNA-based therapies as broadly on the rise in neurodegenerative diseases.
At Quebec conference, researchers considered multiple aspects of herpesvirus biology that may come in to play in AD.
CryoEM helps explain how the inhibitory receptors open and close their ion channels.
In Barcelona, data ran the gamut from a few hopeful little hints on new treatments to mixed signals on familiar players, and failed drugs thrown on the scrap heap.
Can genetics please parse the confusing spectrum of frontotemporal dementias? Whole genome sequences make a start.
The FDA has prioritized review of C2N’s blood test for amyloid-β. A pivotal clinical trial will correlate the test with amyloid PET scans.
With plasma tests performing in AIBL staging, scientists are sharing data across platforms and cohorts, and tackling standardization to avoid time lost to irreproducibility.
Scientists at AD/PD 2019 see a Goldilocks of microglial activation: Both too little and too much is bad in an injured brain. How could a therapy make it just right?
At CTAD, intranasal insulin trial stumbles, pioglitazone gets a postmortem, a RAGE inhibitor tries to hang on.