Can BACE Inhibitors Stage a Comeback?
At AAIC, and a separate BACE symposium, scientists argued the case for resuming evaluation of these drugs in clinical trials.
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At AAIC, and a separate BACE symposium, scientists argued the case for resuming evaluation of these drugs in clinical trials.
At AAIC, secondary endpoint data from the API Colombian study showed trends favoring crenezumab, while people taking gantenerumab in open-label extensions declined more slowly than matched controls.
At the Holloway Summit, scientists, regulatory, and foundation leaders discussed how to advance digital biomarkers from the idea stage into standardized, reliable tools for diagnosis and trials.
The inaugural Holloway Summit, hosted by AFTD, focused on the development of digital health technologies to track the progression of FTD’s myriad manifestations.
In the field's quest for disease-modifying treatments, two different α-synuclein vaccines and two antibodies look promising in preclinical studies, as well.
New, unbiased single-cell methods uncover coordinated changes in cell populations and their interactions. These correlate with disease pathology, progression.
By triggering release of mitochondrial DNA, tau fibrils may set off a cytosolic sensor that activates the interferon response. Blocking this sensor spared neurons and memory in mice.
At AD/PD, some speakers sought to bolster the argument that amyloid removal slows cognitive decline, while others identified what type of patient is most likely to benefit.
At AD/PD, researchers presented pharmacologic analyses that could help predict antibody effects and select the right dosage to keep plaques at bay.
A new tracer detects α-synuclein aggregates in people with multiple system atrophy. Binding is weak, and undetectable in people with other synucleinopathies.
The new vaccine stalled neurodegeneration and improved learning. An antibody that binds the same epitope had similar effects, and only binds soluble oligomers.
Taking a stab at secondary prevention, the four-year Phase 3 trial will assess the antibody’s ability to slow slippage in 1,200 cognitively healthy, amyloid-positive people.
In iPSC-derived cells, H1 risk haplotype is linked to noncoding, antisense variants and to a master regulator of oxidative stress
In two primary tauopathies, natural killer cells invade the brain. In Alzheimer’s, a microglial antiviral response dominates, and hyperexcitability may play a role.
Neurons need LRRK2 in order to take up tau from the extracellular milieu. In ALS neurons, tau scuppers mitochondria, whereas in healthy cells it helps the nucleolus to function correctly.