CTAD Lessons for 2020: More Phase 2 Trials, More Diversity
Besides further broadening the Alzheimer’s therapeutic pipeline, researchers urge a return to Phase 2, using artificial intelligence tools to streamline aspects of trials.
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Besides further broadening the Alzheimer’s therapeutic pipeline, researchers urge a return to Phase 2, using artificial intelligence tools to streamline aspects of trials.
An expanded set of CSF biomarkers exposed tight connections between p-tau, synaptic dysfunction, and neuroinflammation in people with brain amyloid.
Positive allosteric modulators improve learning and memory in mouse models of AD and epilepsy.
In Alzheimer’s brain, granulovacuolar bodies in neurons harbor activated necrosomes. They correlate with tau pathology and neuron loss, raising new questions about how neurons die in this disease.
In early Alzheimer’s disease, the pattern of tau deposition also strongly predicts areas destined for subsequent degeneration.
These oily microglia resemble the foamy macrophages seen in atherosclerotic plaques. They correlate with aging, inflammation, and neurodegenerative disease.
Three studies found no link between vascular disease and cerebral amyloidosis.
At CTAD, researchers discussed possible paths forward. One option: exploring whether low doses prevent plaque accumulation while avoiding the cognitive side effects.
Aβ oligomers latch onto adrenergic receptors, mobilizing a kinase that phosphorylates tau. Blocking adrenergic signaling wards off memory problems in amyloidosis mice.
Aberrant protein-protein interactions centered on HSP90 may contribute to Alzheimer’s disease. Can an inhibitor set things right?
Functional connections between two brain regions are the strongest indicator that pathologic, accumulated tau will spread from one to another.
A small molecule binds the retromer complex, preventing Aβ accumulation, tau hyperphosphorylation, and their downstream consequences in mice.
Frequent heading weakened verbal memory in amateur soccer players, and more so in ApoE4 carriers.
Poor lysosomal function in dopaminergic neurons derived from people with YOPD points to disease origin and potential therapies.
Middle-aged WTC responders have cognitive problems, which correlate not only with their PTSD symptoms and exposure to toxic dust, but also with biomarkers of amyloid and tau.