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.
Small molecules headed for clinical trials target the cell surface protein, displace bound Aβ, and rescue memory in animal models of Alzheimer's.
The ALS/FTD gene produces repeat dipeptides that enter the nucleolus and kill cells within days.
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.
Speakers at CTAD presented new treatment approaches, including a combination of two repurposed drugs that have no activity by themselves.
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.
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.
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.
Tiny spheres full of oxygen soothe neuroinflammation and fight neurodegeneration, researchers reported at SfN. The concept may seem strange, but AD trials are on the horizon.
Scientists claim that MRI detects an Aβ oligomer-specific probe delivered to the mouse brain through the nose.
Researchers mimic neuroprotective RNAs with stable DNAs that can do the same job.
Posing as the amino acid tyrosine, the anti-aging compound resveratrol turns on a new target, PARP1.
Measuring total prion protein in cerebrospinal fluid could help clinicians differentiate between prion disease and rapidly progressing forms of dementia.
Like a second skin, a new kind of neural implant is as compliant as the protective dura membrane that envelops the central nervous system.
Sil1’s presence keeps the endoplasmic reticulum from activating a chronic stress response.
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