News Flash: Colombian Families Come to Phoenix for Amyloid PET
All those who follow the Alzheimer's Prevention Initiative may want to check out a recent New York Times article...
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All those who follow the Alzheimer's Prevention Initiative may want to check out a recent New York Times article...
When the Dominantly Inherited Alzheimer Network gathered at the its hub at Washington University, St. Louis, Missouri, researchers exchanged new science on ARIA...
Researchers have laid out a vision for pre-symptomatic treatment trials that emphasize use of biomarkers to evaluate investigational drugs...
Could it be that a γ-secretase mutation helped give rise to communism?
Mutations in presenilin associated with familial Alzheimer disease perturb calcium signaling in cells. In particular, some mutations suppress...
Scientists propose that Auguste Deter, the first identified Alzheimer disease patient, carried the N141I presenilin-2 mutation...
A new study suggests that early and late-onset forms of Alzheimer's disease may bear little resemblance at the molecular level...
During his lifetime, Alois Alzheimer described five cases of the “characteristic sickness of the cerebral cortex” that his boss, the eminent psychiatrist Emil Kraepelin, later would name in honor of his late colleague. Now, neurologists in Alzheimer’s home state of Bavaria are investigating how these early patients’ family members fared. One patient, Johann F., turns out to have belonged to a large clan afflicted with an early-onset, heritable form of the disease. Many descendants still live in Bavaria, some in the U.S.
The largest meta-analysis done to date confirms dramatic variability in age at onset of autosomal-dominant Alzheimer's disease overall, but finds mutation type and parental age at onset to be strong predictive modulators.
CRISPR-Cas9 gene editing rids embryos of a mutation causing heart disease, evoking a future where autosomal-dominant disease is prevented at the DNA level. What about AD, FTD, and ALS?
Researchers take first steps on road to targeting disease-causing APP mutations and amyloid processing.
Scientists link this mysterious form of dementia to higher plasma LDL-cholesterol, and to genetic variants in APOB, which encodes the major component of low-density lipoprotein.
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.
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.
Comprising mostly Aβ40, these large plaques are shot through with strange tubular structures and BBB markers. They are common in early onset AD.