Different Cellular Mechanisms in Familial and Sporadic Alzheimer’s?
A single-nuclei RNA-Seq study found more autophagy and chaperone gene expression in familial AD brain, more intense microglial activation in sporadic.
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A single-nuclei RNA-Seq study found more autophagy and chaperone gene expression in familial AD brain, more intense microglial activation in sporadic.
In mice, these Aβ fibrils avoid riling microglia and astrocytes. They also evade both PiB and lecanemab.
Among 1,092 people with PCA, symptoms started around age 60, and 94 percent had amyloid plaques or neurofibrillary tangles.
Eight adults who, as children, had received growth hormone from cadavers developed cognitive problems and/or AD-like pathology in midlife.
A U.K. Biobank analysis generated 15 risk factors for young-onset dementia. Many factors also correlated with late-onset disease.
Twelve people heterozygous for this protective variant were still sharp seven years after their expected age of AD onset. One had fewer tangles than expected.
First data from the Longitudinal Early-Onset Alzheimer’s Disease Study hints at what might cause this type of AD and how it unfolds.
While each disease features distinct proteomes in the brain, cerebrospinal fluid, and blood, some proteins overlap. They are more dysregulated in familial than in sporadic AD.
An amino acid change in this ApoE receptor-binding protein may have bestowed 20 years of resilience to a brother and sister carrying the presenilin Paisa mutation.
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.
Topline results showed no statistically significant slowing of decline on either of two primary endpoints. Trends across multiple endpoints favored crenezumab.
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.
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.
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.
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.