Hats Off to ApoE—Key to Formation of Functional Amyloid
Lipoprotein cap on pigment cell exosomes is essential for production of an amyloid scaffold that concentrates melanin.
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Lipoprotein cap on pigment cell exosomes is essential for production of an amyloid scaffold that concentrates melanin.
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.
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.
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.
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.
Using creative ways of mining genetic data, researchers are coming up with new risk variants for Alzheimer’s.
Chemical mutagenesis yields an SOD1 variant found in people with the disease. Neurons degenerate without overexpression of the enzyme.
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.
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.
The ALS/FTD gene produces repeat dipeptides that enter the nucleolus and kill cells within days.
Speakers at CTAD presented new treatment approaches, including a combination of two repurposed drugs that have no activity by themselves.
When provoked by Aβ, astrocytes unleash a torrent of inflammatory signals. Under it, neuronal dendrites wither and lingering synapses turn hyperactive.
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.