Using Lecanemab Trial Data to Determine Maintenance Dose
At AD/PD, researchers presented pharmacologic analyses that could help predict antibody effects and select the right dosage to keep plaques at bay.
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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.
Mild COVID Infection Can Shrink Brain, Speed Cognitive Decline
In some people who had weathered COVID at home, olfactory regions in the brain shrank and executive function slowed. Will these changes resolve or persist?
Are Mid-Life Depression and Anxiety Early Signs of Alzheimer’s?
CSF Aβ and tau are abnormal in older people with psychiatric problems. Are these symptoms an effect of AD pathogenesis, or risk factors for it?
In Familial AD, Amyloid-PET Varies by Mutation Type; CSF Aβ42 Doesn't
A person's burden and spatial distribution of plaques, as measured by PiB-PET, varied greatly depending on his or her mutation. Their CSF Aβ42 or cognitive decline did not.
BDNF Val66Met Hastens Tau Phosphorylation in Familial Alzheimer’s
APP or presenilin mutation carriers who also carried the Met66 allele had more p-tau217 at presymptomatic stages, and more p-tau205 at symptomatic stages, than did Val carriers.
Identical Twins Share Tau Trajectory, but Lifestyle Can Make a Difference
Among 39 sets of identical twins, tau tangles accumulated in a strikingly similar pattern within each pair. A pair's discordance was due to Aβ and factors such as exercise.
2021—A Turning Point for Alzheimer’s Research and Therapy?
Alzforum editors review the highlights of last year’s clinical and research developments.
Amyloid Alone—Any Amyloid—Raises P-Tau in Mice
Cerebrospinal fluid p-tau217 and -181 rose in tandem with amyloid deposition in the brain, regardless of whether the plaques contained Aβ or amyloid formed by a different protein.
Does More Aβ38 Mean Less Cognitive Decline in Alzheimer’s?
People with subjective or mild cognitive impairment are less likely to get dementia if their CSF Aβ38 levels are high. Should γ-secretase modulators be revived?
In Preclinical Alzheimer's, p-tau217 in Blood Best Predicts Tangles
Tau PET holds a slight edge over the plasma marker in people who already have mild cognitive impairment.
Bringing Alzheimer’s Detection into the Digital Age
At CTAD, scientists presented an electronic version of the CDR, plus new digital tests. Will smartphone apps pick up mild cognitive impairment and even preclinical cognitive change?
The Rain in Spain: Move Over Higgins, AI Spots Speech Patterns
AI-powered apps catch changes in how a person speaks that may reveal cognitive decline in frontotemporal dementia and early Alzheimer’s. Can smartphones deliver biomarkers for trial enrollment and diagnosis?
Plasma Aβ—First Sign of AD, But Tough to Measure Prospectively?
Data shown at CTAD suggests the Aβ42/40 ratio falls in the blood before it does in the CSF, offering perhaps the earliest glimpse at the pathophysiology of Alzheimer's. Measuring that change prospectively might be a tall order.
Donanemab Phase 3 Puts Plasma p-Tau, Remote Assessments to the Test
At CTAD, all eyes were on the anti-amyloid antibody donanemab, which is before the FDA. Scientists showed how Phase 3 is enrolling, and how plasma tau enables wholly remote inclusion of people with plaques and tangles.
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