Implicated in ARIA: Perivascular Macrophages and Microglia
These immune cells spew free radicals and inflammatory cytokines that damage blood vessels, contributing to edema and brain bleeds.
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These immune cells spew free radicals and inflammatory cytokines that damage blood vessels, contributing to edema and brain bleeds.
Case studies from the Dominantly Inherited Alzheimer Network trial show amyloid immunotherapy can prevent tangles and cognitive decline in some mutation carriers.
On gantenerumab, some people with dominantly inherited AD mutations remain plaque- and tangle-free, and cognitively healthy, years after their expected age of onset.
People who sifted through piles of debris are nine times likelier to develop early onset, all-cause dementia than those exposed to little toxic dust.
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.