In 2,144 Colombian ADAD family members, plasma NfL in gene carriers rises as early as two decades before their symptoms start.
At AAIC, researchers presented baseline data from an ongoing, five-year study asking whether the anti-Aβ antibody crenezumab can forestall cognitive decline in autosomal-dominant Alzheimer’s disease.
A brother’s survival guilt, a journalist tracing her mutation to Lebanon, a student freezing her eggs ahead of a primary prevention trial—DIAN family members are stirring their growing community to act against Alzheimer’s disease.
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.
Presented at AD/PD, the discovery by scientists in Uppsala is the first APP deletion found to cause Alzheimer’s disease. The same group found the Swedish and Arctic APP mutations.
In familial Alzheimer’s disease, rise in NfL in the blood precedes disease onset by 16 years.
In DIAN, participants who are more physically active may also have slower disease progression.
Recent studies have identified rare loss-of-function variants that cause Alzheimer’s with nearly 100 percent penetrance. Now there are 17 more.
Researchers take first steps on road to targeting disease-causing APP mutations and amyloid processing.
A comparison of these large data sets shows that while the two forms of Alzheimer’s disease have separate triggers, they follow the same course and are much more similar than different.
Health records from 31 million French people suggest that drinking to excess is a major risk factor for early onset dementia.
In people with an autosomal-dominant AD mutation, Aβ and tau start accumulating long before the estimated onset of symptoms.
The neurodegeneration marker appears to track disease severity in AD and MS patients with great sensitivity.
Rather than changing one by one, many biomarkers—including cognition, tau PET, hippocampal atrophy, and CSF p-tau—shift together, around the time of symptom onset in young adults with familial AD.
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?