API Colombian Trial of Crenezumab Missed Primary Endpoints
Topline results showed no statistically significant slowing of decline on either of two primary endpoints. Trends across multiple endpoints favored crenezumab.
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Presenilin Mutations Stall Endosomal Transport, Swell Axons
In neurons lacking PS1, late endosomes get bogged down by imbalanced calcium. This puts kinases in a tizzy, slows motor proteins, and makes neurites dystrophic.
Robust TREM2 Expression May Delay Alzheimer’s Disease
In familial AD, the faster sTREM2 rises in a person's cerebrospinal fluid, the slower his or her amyloid grows, cortex thins, and cognition fades.
Lecanemab Sweeps Up Toxic Aβ Protofibrils, Catches Eyes of Trialists
In a comparison with aducanumab and gantenerumab, lecanemab mopped up protofibrils most efficiently; the antibody has been chosen for DIAN-TU and AHEAD 3-45 trials.
Double Whammy: APP Uppsala Deletion Ups Aβ and Its Aggregation Propensity
Found in one Swedish family, this mutation speeds up plaque deposition by way of two different mechanisms, leading to disease onset as young as age 40.
Estimates of Young-Onset Dementia Prevalence Just Doubled
A meta-analysis of 2.8 million people estimates 119 in 100,000 develop dementia before age 64—twice the previous estimates. Prevalence increases with age and strikes men and women equally.
Aiming at the Tangle’s Heart? DIAN-TU Trial to Torpedo Tau’s Core
The global platform trial for Alzheimer’s due to mutations in APP or presenilin will try to treat or prevent symptoms by deploying a therapeutic antibody that homes in on a piece of tau known to aggregate into neurofibrillary tangles.
Are the Long Aβ Peptides the Real Bad Guys?
Among 14 familial Alzheimer’s APP mutations, two don’t change the Aβ42/Aβ40 ratio, but all of them yield long peptides of 45 to 49 residues that hide out in the membrane.
Introducing the Coarse-Grained Plaque—A New Type of Amyloid
Comprising mostly Aβ40, these large plaques are shot through with strange tubular structures and BBB markers. They are common in early onset AD.
Umbilical Cord With Presenilin Mutation Births New Cell Model of Familial AD
Umbilical cord stem cells from presenilin 1 E280A carriers, once differentiated into cholinergic-like neurons, pumped out Aβ42 and accumulated phosphorylated tau and apoptotic markers.
Mutations in Epigenetic Gene Linked to Neurodegeneration
Loss-of-function variants in the demethylase TET2 raise a person’s risk for early and late-onset Alzheimer’s, as well as FTD and ALS, suggesting a common mechanism.
Confused About the DIAN-TU Trial Data? Experts Discuss
The AAT-AD/PD conference hosted a virtual conversation about what the trial’s disappointing cognitive and tantalizing biomarker data might mean. Hidden between thank you’s and pledges to stay committed were substantive points of debate and context.
In DIAN-TU, Gantenerumab Brings Down Tau. By a Lot. Open Extension Planned
Data shown at AAT-AD/PD explain why the DIAN-TU trial missed its primary endpoint. But gantenerumab strongly reduced plaques, tau, phospho-tau, and slowed NfL. This result prompted an open-label extension, sustaining hope for efficacy.
Different CSF Phospho-Taus Match Distinct Changes in Brain Pathology
Different forms of p-tau in cerebrospinal fluid reflect worsening plaque load, metabolism, and atrophy in the brain. They could help stage Alzheimer’s disease.
Topline Result for First DIAN-TU Clinical Trial: Negative on Primary
DIAN, Roche, Lilly disclose that neither gantenerumab nor solanezumab slowed cognitive decline in the first-pass comparison of drug and placebo groups. Analyses are ongoing; dose may have been too low.
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