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.
The amino terminus toggles between a neatly folded nucleic acid-binding domain and a disorganized configuration that forms inclusions.
Tiny secreted vesicles emerge as important players in communication between brain cells. Are they important in neurodegeneration?
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 The development of the next generation of Alzheimer’s disease ...
A sense of change on all fronts pervaded the Clinical Trials on Alzheimer’s Disease conference. Scientists shared their early experiences of what works and what does not as they begin trials with newly defined cohorts, new diagnostic criteria, and new outcomes.
After lighting up microglia in mouse models of AD, a tracer is headed for clinical trials.
Medication blocks molecular transporters that eject riluzole from the nervous system.
Protein touted as a peripheral monocyte receptor that worsens amyloid plaque pathology in transgenic mice.
High doses of BACE1 inhibitors stymie synaptic activity in mice. Researchers recommend careful dosing in clinical trials.
Having variants in three, or even two, genes for amyotrophic lateral sclerosis brings on symptoms a decade earlier. This also happens in sporadic cases, bringing the very term into question, researchers say.
A study in a mouse model of Alzheimer’s disease proposes that degenerating neurons become more excitable because they lose dendrites.
A micro-immunoelectrode allows researchers measure Aβ levels in the interstitial fluid of mice every 30 seconds.