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.
Speakers at CTAD presented new treatment approaches, including a combination of two repurposed drugs that have no activity by themselves.
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.
Using creative ways of mining genetic data, researchers are coming up with new risk variants for Alzheimer’s.
Researchers at CTAD announced the end for two active immunotherapies, along with the curious story of a placebo as a treatment and the start of a new antibody.
Researchers at CTAD reported seeing biomarkers budge in active and passive immunotherapy trials, but measurement techniques and screening protocols still need improvement for early stage trials to succeed.
A CAP symposium opened the CTAD conference, indicating that presymptomatic treatment and “federated” research have become mainstream thinking in Alzheimer’s therapy development. EPAD is pulling together European sites.
At CTAD, former FDA neurology leader Rusty Katz urged Alzheimer’s trialists to stop fussing over disease progression. He recommended going after a large effect, regardless of whether it can garner a label of disease modification. That, he says, may mean combination trials.
Lipoprotein cap on pigment cell exosomes is essential for production of an amyloid scaffold that concentrates melanin.
A new trend in cell biology points to vesicles released from cells as agents that form and spread pathogenic proteins.