CTAD Shows Alzheimer’s Field Trying to Reinvent Itself Rusty Unleashed: Forget Disease Modification, Go For Big Effect From Shared CAP, Secondary Prevention Trials are Off and Running Immunotherapy I: Baby Steps, but No Breakthroughs Immunotherapy II: ...
In mouse models of AD, one astrocyte purinergic receptor makes glia hyperactive, while another may suppress memory. Both are upregulated in the AD brain, researchers report.
Researchers at CTAD added to growing evidence that brain amyloid accumulation presages cognitive decline, although several different factors influence how fast that decline will happen in a given person.
At CTAD 2014, potential drugs for agitation, aggression, and other psychiatric symptoms of Alzheimer’s disease emerged as a prominent theme.
Scientists are finding how calcium dysregulation in mouse models of Alzheimer’s shrivels synapses and impairs neural plasticity, with effects that extend to the network level.
When provoked by Aβ, astrocytes unleash a torrent of inflammatory signals. Under it, neuronal dendrites wither and lingering synapses turn hyperactive.
Speakers at CTAD presented new treatment approaches, including a combination of two repurposed drugs that have no activity by themselves.
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.