PET scans indicate no more AD pathology in PD-MCI than healthy controls, suggesting their cognitive decline results from other factors.
Ephemeral as they may be, these maligned peptides have become the targets of small-molecule and immunotherapies. Initial results of these efforts to catch and remove Aβ oligomers are trickling in.
Phase 1 trial tests the rejuvenating effects of young blood, while albumin replacement may offer its own benefits.
According to a press release by trial sponsor Ionis, therapy was well tolerated, but trial results have yet to be released.
In a Phase 2 trial in nursing home residents with Alzheimer’s, this new drug mitigated symptoms safely, without detriment to cognition.
Gradually raising the dose of this therapeutic antibody appears to ease the risk of brain inflammation.
Presented at CTAD, BACE inhibitor’s efficacy and safety results in mild to moderate AD were encouraging to some clinicians, vaguely disquieting to others.
Recruitment, recruitment, recruitment: Registries get creative in how they promote research engagement and fill prevention trials.
At CTAD, well over a dozen drug trials reported results. One of the more radically new approaches is to bring to bear the health benefits of young blood—even though they are far from fully understood in molecular terms—on an old brain struggling with neurodegeneration. How is that going? In a first Phase 1 trial, the approach seemed safe, and a newer young blood fraction is being put to the test next.
In a Phase 2 trial, the serotonin receptor antagonist mitigated symptoms of psychosis in people with advanced AD, with a good safety profile and no deleterious effect on cognition. Better drugs are needed to replace traditional antipsychotics, whose use in dementia patients brings little benefit and much risk.
With more, larger, and earlier stage clinical trials coming online for Alzheimer’s disease, researchers are hitting a recruitment bottleneck. How to find people in their 50s and 60s who do not yet know they may be on the path to Alzheimer’s? Online registries, local ApoE genotyping parties, booths at community events, deeply phenotyped cohorts, electronic health records—a variety of approaches are being explored to engage potential participants and massively increase the number of people joining prevention research. Is it working? Read our CTAD update.
To improve cognitive testing, go digital, go home, and test yourself often. That’s according to researchers at the recent CTAD conference in Boston. A smartphone app that allows frequent, brief evaluations in the course of daily life dramatically increased the reproducibly of cognitive testing over in-clinic test sessions. A digital pen turned the old-fashioned clock-drawing test into a sensitive detector of subtle cognitive impairment. Both approaches should help efforts to find and follow people with the earliest signs of AD for prevention and treatment trials. In turn, trials should suss out participants’ rates of decline with frequent measures.
Tau PET is emerging as the favored biomarker to gauge disease progression for AD trials, according to researchers gathered at the 10th Clinical Trials on Alzheimer’s Disease conference in Boston. For AD and other tauopathies, the Piramal probe looks promising and a Merck compound is preparing to burst on the scene. New data offer a first look at PET measurements of synaptic loss.
- Kejal Kantarci on Aβ, Tau Absolved of Causing Mild Cognitive Impairment in Parkinson’s
- Tiago Outeiro on Aβ, Tau Absolved of Causing Mild Cognitive Impairment in Parkinson’s
- Stephen Gomperts on Aβ, Tau Absolved of Causing Mild Cognitive Impairment in Parkinson’s
- Allan Hansen on Aβ, Tau Absolved of Causing Mild Cognitive Impairment in Parkinson’s
- Susanne Aileen Funke on From New Tau Structure, Bona Fide Aggregation Inhibitors?
- Rachel Bennett on Aβ Plaques: Breeding Ground for Toxic Tau?
- Takaomi Saido on Aβ Plaques: Breeding Ground for Toxic Tau?
- Susana Pinto on In ALS, Respiratory Measure Predicts Pace of Disease
- Robert Friedland on Paper Alert: Aβ Fibril Structures Vary by AD Subtype
- Marcus Raichle on Daydreaming Network Serves as Ground Zero for Aβ Deposition
- Nicholas Seyfried on Stress Granule Protein Stabilizes Tau Oligomers, Hastens Neurodegeneration
- Takaomi Saido on Serum NfL Detects Preclinical AD, Reflects Clinical Benefit
- Joe Abisambra on Stress Granule Protein Stabilizes Tau Oligomers, Hastens Neurodegeneration
- Aaron Gitler on Stress Granule Protein Stabilizes Tau Oligomers, Hastens Neurodegeneration
- Petra Kashi on Inflammation in Midlife Portends Late-Life Brain Shrinkage
- Dinesh Dhull on Peripheral Aβ Can Accumulate in Brain, Trigger Degeneration
- Peter Nelson on Distinct Cognitive Fates in the Very Old
- Delphine Boche and Clive Holmes on Inflammation in Midlife Portends Late-Life Brain Shrinkage
- Tom Mosley on Inflammation in Midlife Portends Late-Life Brain Shrinkage
- Douglas Galasko on Serum NfL Detects Preclinical AD, Reflects Clinical Benefit
- Yan-Jiang Wang on Peripheral Aβ Can Accumulate in Brain, Trigger Degeneration