Roughly at its halfway point, a trial of a therapeutic Aβ antibody is over. Data aren’t out yet, but scientists suspect gantenerumab may have been dosed based on safety, too low to achieve an efficacious dose in the brain.
The ALS/FTD gene produces repeat dipeptides that enter the nucleolus and kill cells within days.
Small molecules headed for clinical trials target the cell surface protein, displace bound Aβ, and rescue memory in animal models of Alzheimer's.
New therapeutics such as plant-based estrogens and neurosteroids caught notice at CTAD as an approach to try to prevent cognitive decline in women who metabolic markers indicate may be at risk for Alzheimer's.
Internet and tablet-based cognitive tests were trendy at CTAD. If they prove their worth, they may provide a quicker and cheaper way to screen large numbers of people for trials, and track cognitive decline more accurately.
Researchers at CTAD advanced tau research on several fronts, correlating tau PET with Braak stage and memory loss, and introducing a new tau model and therapeutic antibody.
Chemical mutagenesis yields an SOD1 variant found in people with the disease. Neurons degenerate without overexpression of the enzyme.
Using creative ways of mining genetic data, researchers are coming up with new risk variants for Alzheimer’s.
Held in a historic skyscraper built in 1932 for a Philadelphia bank, the seventh conference on Clinical Trials on Alzheimer’s Disease drew 715 scientists to this city between November 20 and 22. CTAD featured a sprinkling of new trial results and enthusiasm about treating agitation in AD, but most of the activity reflected a field trying to rebuild itself from the ground up. Trialists swapped notes on implementing new diagnostic criteria in therapy trials, enriching trial populations, and exploring home-based assessments and other tools to support prevention trials. Secondary prevention sounded positively mainstream and has become the stuff of large-scale collaborations. Rusty Katz, formerly of the FDA, implored trialists to stop obsessing over disease modification and to aggressively go after big therapeutic effects instead. Those, Katz said, may require a commitment to co-develop combinations of investigational drugs. Read Madolyn Rogers and Gabrielle Strobel’s series in the coming days.
Scientists know little about sigma2, but it seems to stabilize a variety of receptors on the cell surface. Might it also partner with Aβ? At this year's Society for Neuroscience annual meeting, held November 15 to 19 in Washington, D.C., scientists from Pittsburgh-based Cognition Therapeutics claimed that sigma2 mediates Aβ binding to neurons, and that allosteric modulators of the receptor protect against Aβ toxicity, even displacing the peptide from human brain tissue. The company hopes to take this compound into clinical trials.
- Dieter Edbauer on Antisense Proline-Arginine RAN Dipeptides Linked to C9ORF72-ALS/FTD Form Toxic Nuclear Aggregates that Initiate In Vitro and In Vivo Neuronal Death.
- Iryna Benilova on Meet Sigma2, a New Aβ Receptor?
- Martin Citron on Pharmacological Inhibition of Beta Site Amyloid Precursor Protein Cleaving Enzyme 1 Can Impair Synaptic Plasticity and Specific Cognitive Functions
- Stefan Lichtenthaler on Pharmacological Inhibition of Beta Site Amyloid Precursor Protein Cleaving Enzyme 1 Can Impair Synaptic Plasticity and Specific Cognitive Functions
- Michael van Es on Amyotrophic lateral sclerosis onset is influenced by the burden of rare variants in known amyotrophic lateral sclerosis genes.
- Marc Aurel Busche on Dendritic structural degeneration is functionally linked to cellular hyperexcitability in a mouse model of Alzheimer's disease.
- Igor Timofeev on Dendritic structural degeneration is functionally linked to cellular hyperexcitability in a mouse model of Alzheimer's disease.